Chikenji Takako S.

Faculty of Health Sciences　Health Sciences　Department of Rehabilitation ScienceProfessor
Institute for the Advancement of Higher EducationProfessor
Last Updated :2025/06/12

■Researcher basic information

Degree

  • Ph.D

Researchmap personal page

Home Page URL

Researcher number

  • 40452982

ORCID ID

J-Global ID

Research Keyword

  • Tissue regeneration
  • Cell senescence
  • Chronic inflammation
  • autoimmune disease
  • 慢性腎臓病
  • 間葉系幹細胞
  • Fibrosis

Research Field

  • Life sciences, Nutrition and health science
  • Life sciences, Anatomy
  • Life sciences, Orthopedics
  • Life sciences, Rehabilitation science

Educational Organization

■Career

Career

  • Apr. 2021 - Present
    Hokkaido University, Faculty of Health Sciences, Professor
  • Apr. 2019 - Mar. 2021
    Hokkaido University, 保健科学研究院, Associate professor
  • Jul. 2018 - Jun. 2019
    Mayo Clinic, Research fellow
  • Oct. 2014 - Jul. 2018
    Sapporo Medical University School of Medicine, Department of Anatomy, Assistant professor
  • Apr. 2013 - Sep. 2014
    Sapporo Medical University, School of Health Sciences, 助教
  • 2010 - 2012
    Mayo Clinic Research Fellow

■Research activity information

Awards

  • Jun. 2020, 北海道大学大学院保健科学研究院, 優秀論文賞　　　　　　　　　　　　　　　
  • Feb. 2020, Orthopedics Research Society, 2020 New Investigator Recognition Award (NIRA), Corresponding author　　　　　　　　　　　　　　　

Papers

  • HLA class I-downregulated senescent epidermal basal cells orchestrate skin pathology in cutaneous lupus erythematosus.
    Sena Yamamoto, Yuki Saito, Tsukasa Sato, Seina Nakano, Dain Kasseki, Ayaka Nagao, Norihiro Miura, Kentaro Nagaoka, Arisa Kita, Maki Miyajima, Shogo Ijima, Koji Taniguchi, Atsushi Niida, Takako S Chikenji
    Arthritis & rheumatology (Hoboken, N.J.), 19 May 2025, [Peer-reviewed], [Last author, Corresponding author], [International Magazine]
    English, Scientific journal, OBJECTIVE: To investigate the role of senescent epidermal basal cells in cutaneous lupus erythematosus (CLE) pathogenesis using skin samples from patients with CLE and a mouse model of systemic lupus erythematosus (SLE). METHODS: Cellular senescence profiling utilized datasets from the NCBI Gene Expression Omnibus database and Accelerating Medicines Partnership® (AMP®) Phase 1-Metro. Gene array data from GSE184989 (CLE: n = 68, control: n = 4), single-cell RNA sequencing data from GSE186476 (CLE: n = 7, control: n = 14), and AMP® Phase 1-Metro (SLE: n = 17) were utilized. In vitro experiments further examined the expression of p21WAF1/CIP1, type I interferon (IFN), human leukocyte antigen class I (HLA-I), and epidermal growth factor receptor (EGFR) signalling. Pharmacological clearance of senescent cells was performed using the senolytic drug fisetin in the SLE mouse model. RESULTS: p21WAF1/CIP1-high senescent epidermal basal cells in patients with CLE exhibit high type I IFN expression. These cells enhance IFN signalling in surrounding normal epidermal basal cells, leading to increased HLA-I expression. In contrast, senescent epidermal cells upregulate EGFR signalling, which downregulates HLA-I expression, allowing them to evade immune surveillance. This heterogeneity of HLA-I expression promotes CD8-positive T-mediated toxicity against normal epidermal basal cells, resulting in their apoptosis. Pharmacological clearance of senescent epidermal basal cells improved SLE-like skin lesions. CONCLUSION: Senescent cells create a microenvironment that directs cytotoxic T-cell-mediated responses against normal epidermis in CLE, contributing to disease pathology. Targeting senescent cells and their signalling pathways may offer novel therapeutic strategies for CLE and SLE skin lesions.
  • Role of cellular senescence in inflammation and regeneration
    Yuki Saito, Sena Yamamoto, Takako S. Chikenji
    Inflammation and Regeneration, 44, 1, Springer Science and Business Media LLC, 03 Jun. 2024, [Invited], [Last author, Corresponding author], [International Magazine]
    Scientific journal, Abstract

    Cellular senescence is the state in which cells undergo irreversible cell cycle arrest and acquire diverse phenotypes. It has been linked to chronic inflammation and fibrosis in various organs as well as to individual aging. Therefore, eliminating senescent cells has emerged as a potential target for extending healthy lifespans. Cellular senescence plays a beneficial role in many biological processes, including embryonic development, wound healing, and tissue regeneration, which is mediated by the activation of stem cells. Therefore, a comprehensive understanding of cellular senescence, including both its beneficial and detrimental effects, is critical for developing safe and effective treatment strategies to target senescent cells. This review provides an overview of the biological and pathological roles of cellular senescence, with a particular focus on its beneficial or detrimental functions among its various roles.
  • Cellular senescence and wound healing in aged and diabetic skin
    Arisa Kita, Sena Yamamoto, Yuki Saito, Takako S. Chikenji
    Frontiers in Physiology, 15, Frontiers Media SA, 19 Feb. 2024, [Peer-reviewed], [Last author, Corresponding author]
    Scientific journal, Cellular senescence is a biological mechanism that prevents abnormal cell proliferation during tissue repair, and it is often accompanied by the secretion of various factors, such as cytokines and chemokines, known as the senescence-associated secretory phenotype (SASP). SASP-mediated cell-to-cell communication promotes tissue repair, regeneration, and development. However, senescent cells can accumulate abnormally at injury sites, leading to excessive inflammation, tissue dysfunction, and intractable wounds. The effects of cellular senescence on skin wound healing can be both beneficial and detrimental, depending on the condition. Here, we reviewed the functional differences in cellular senescence that emerge during wound healing, chronic inflammation, and skin aging. We also review the latest mechanisms of wound healing in the epidermis, dermis, and subcutaneous fat, with a focus on cellular senescence, chronic inflammation, and tissue regeneration. Finally, we discuss the potential clinical applications of promoting and inhibiting cellular senescence to maximize benefits and minimize detrimental effects.
  • Senescence-associated secretory phenotypes in mesenchymal cells contribute to cytotoxic immune response in oral lichen planus.
    Shogo Ijima, Yuki Saito, Sena Yamamoto, Kentaro Nagaoka, Taiki Iwamoto, Arisa Kita, Maki Miyajima, Tsukasa Sato, Akihiro Miyazaki, Takako S Chikenji
    Immunity & ageing : I & A, 20, 1, 72, 72, 05 Dec. 2023, [Peer-reviewed], [Last author, Corresponding author], [International Magazine]
    English, Scientific journal, Oral lichen planus is a chronic inflammatory condition that adversely affects the oral mucosa; however, its etiology remains elusive. Consequently, therapeutic interventions for oral lichen planus are limited to symptomatic management. This study provides evidence of the accumulation of senescent mesenchymal cells, CD8 + T cells, and natural killer cells in patients with oral lichen planus. We profiled the patients' tissues using the National Center for Biotechnology Information Gene Expression Omnibus database and found that senescence-related genes were upregulated in these tissues by gene set enrichment analysis. Immunohistochemical analysis showed increased senescent mesenchymal cells in the subepithelial layer of patients with oral lichen planus. Single-cell RNA-seq data retrieved from the Gene Expression Omnibus database of patients with oral lichen planus revealed that mesenchymal cells were marked by the upregulation of senescence-related genes. Cell-cell communication analysis using CellChat showed that senescent mesenchymal cells significantly influenced CD8 + T cells and natural killer cells via CXCL12-CXCR4 signaling, which is known to activate and recruit CD8 + T cells and NK cells. Finally, in vitro assays demonstrated that the secretion of senescence-associated factors from mesenchymal cells stimulated the activation of T cells and natural killer cells and promoted epithelial cell senescence and cytotoxicity. These findings suggest that the accumulation of mesenchymal cells with senescence-associated secretory phenotype may be a key driver of oral lichen planus pathogenesis.
  • Intrathecal Injection of Mesenchymal Stromal Cell Cultured on 3D Fiber Ameliorates Multiple Organ Damage in Murine Lupus
    Yuki Saito, Maki Miyajima, Sena Yamamoto, Norihiro Miura, Tsukasa Sato, Arisa Kita, Shogo Ijima, Mineko Fujimiya, Takako S Chikenji
    Stem Cells Translational Medicine, Oxford University Press (OUP), 25 Apr. 2022, [Peer-reviewed], [Last author, Corresponding author], [International Magazine]
    Scientific journal, Abstract

    Up to 60% of patients with systemic lupus erythematosus (SLE) experience autonomic symptom. Sympathetic nervous system damage can cause dysfunction of the bone marrow that activates inflammatory cells, potentially causing multiple organ damage. We hypothesized that sympathetic nervous system damage would induce bone marrow dysfunction with multiple organ damage in SLE, and that multiple organ damage could be improved by therapy targeting the nervous system. Here, we showed that damage to autonomic nerves and Schwann cells occurred in the bone marrow and central nervous system of SLE model mice. A neurotoxic drug increased mortality and induced severe neuropathy and multiple organ damage, while a neuroprotective drug prevented multiple organ damage. The administration of bone marrow-derived mesenchymal stromal cells (BMSCs) cultured on a 3-dimensional fiber scaffold improved bone marrow neuropathy, skin lesions, kidney function, and mortality. Our results reveal that bone marrow neuropathy influence multiple organ damage associated with SLE, and improvement of bone marrow neuropathy by intrathecal injection of BMSC may be a target for SLE multiple-organ damage.
  • Altered regulation of mesenchymal cell senescence in adipose tissue promotes pathological changes associated with diabetic wound healing
    Arisa Kita, Yuki Saito, Norihiro Miura, Maki Miyajima, Sena Yamamoto, Tsukasa Sato, Takatoshi Yotsuyanagi, Mineko Fujimiya, Takako S. Chikenji
    Communications Biology, 5, 1, Springer Science and Business Media LLC, Apr. 2022, [Peer-reviewed], [Last author, Corresponding author], [International Magazine]
    Scientific journal, Abstract

    Pathologic diabetic wound healing is caused by sequential and progressive deterioration of hemostasis, inflammation, proliferation, and resolution/remodeling. Cellular senescence promotes wound healing; however, diabetic wounds exhibit low levels of senescent factors and accumulate senescent cells, which impair the healing process. Here we show that the number of p15INK4B + PDGFRα + senescent mesenchymal cells in adipose tissue increases transiently during early phases of wound healing in both non-diabetic mice and humans. Transplantation of adipose tissue from diabetic mice into non-diabetic mice results in impaired wound healing and an altered cellular senescence–associated secretory phenotype (SASP), suggesting that insufficient induction of adipose tissue senescence after injury is a pathological mechanism of diabetic wound healing. These results provide insight into how regulation of senescence in adipose tissue contributes to wound healing and could constitute a basis for developing therapeutic treatment for wound healing impairment in diabetes.
  • Fisetin reduces the senescent tubular epithelial cell burden and also inhibits proliferative fibroblasts in murine lupus nephritis.
    Shogo Ijima, Yuki Saito, Kentaro Nagaoka, Sena Yamamoto, Tsukasa Sato, Norihiro Miura, Taiki Iwamoto, Maki Miyajima, Takako S Chikenji
    Frontiers in immunology, 13, 960601, 960601, 2022, [Last author, Corresponding author], [International Magazine]
    English, Scientific journal, Systemic lupus erythematosus (SLE) is a chronic autoimmune inflammatory disease characterized by the involvement of multiple organs. Lupus nephritis (LN) is a major risk factor for overall morbidity and mortality in SLE patients. Hence, designing effective drugs is pivotal for treating individuals with LN. Fisetin plays a senolytic role by specifically eliminating senescent cells, inhibiting cell proliferation, and exerting anti-inflammatory, anti-oxidant, and anti-tumorigenic effects. However, limited research has been conducted on the utility and therapeutic mechanisms of fisetin in chronic inflammation. Similarly, whether the effects of fisetin depend on cell type remains unclear. In this study, we found that LN-prone MRL/lpr mice demonstrated accumulation of Ki-67-positive myofibroblasts and p15INK4B-positive senescent tubular epithelial cells (TECs) that highly expressed transforming growth factor β (TGF-β). TGF-β stimulation induced senescence of NRK-52E renal TECs and proliferation of NRK-49F renal fibroblasts, suggesting that TGF-β promotes senescence and proliferation in a cell type-dependent manner, which is inhibited by fisetin treatment in vitro. Furthermore, fisetin treatment in vivo reduced the number of senescent TECs and myofibroblasts, which attenuated kidney fibrosis, reduced senescence-associated secretory phenotype (SASP) expression, and increased TEC proliferation. These data suggest that the effects of fisetin vary depending on the cell type and may have therapeutic effects in complex and diverse LN pathologies.
  • Accumulation of Senescent Neural Cells in Murine Lupus With Depression-Like Behavior
    Yuki Saito, Maki Miyajima, Sena Yamamoto, Tsukasa Sato, Norihiro Miura, Mineko Fujimiya, Takako S. Chikenji
    Frontiers in Immunology, 12, 692321, 692321, Frontiers Media SA, 03 Nov. 2021, [Peer-reviewed], [Last author, Corresponding author], [International Magazine]
    English, Scientific journal, Neuropsychiatric manifestations targeting the central, peripheral, and autonomic nervous system are common in systemic lupus erythematosus (SLE); collectively, these symptoms are termed neuropsychiatric SLE (NPSLE). Among a wide variety of neuropsychiatric symptoms, depression is observed in about 24-39% of SLE patients. Several cytokines and chemokines have been identified as biomarkers or therapeutic targets of NPSLE; in particular, the levels of type 1 interferons, TNFs, and IL-6 are elevated in SLE patient’s cerebrospinal fluid (CSF), and these factors contribute to the pathology of depression. Here, we show that senescent neural cells accumulate in the hippocampal cornu ammonis 3 (CA3) region in MRL/lpr SLE model mice with depressive behavior. Furthermore, oral administration of fisetin, a senolytic drug, reduced the number of senescent neural cells and reduced depressive behavior in the MRL/lpr mice. In addition, transcription of several senescence and senescence-associated secretory phenotype (SASP) factors in the hippocampal region also decreased after fisetin treatment in the MRL/lpr mice. These results indicate that the accumulation of senescent neural cells in the hippocampus plays a role in NPSLE pathogenesis, and therapies targeting senescent cells may represent a candidate approach to treat NPSLE.
  • U-39最先端研究紹介 骨格筋間葉系前駆細胞の細胞老化と骨格筋の再生　　　　　　　　　　　　　　　
    齋藤 悠城, 藤宮 峯子, 千見寺 貴子
    日本基礎理学療法学会学術大会プログラム・抄録集, 26回, シンポジウム2, シンポジウム2, (一社)日本基礎理学療法学会, Oct. 2021
    Japanese
  • Diverse Roles of Cellular Senescence in Skeletal Muscle Inflammation, Regeneration, and Therapeutics
    Yuki Saito, Takako S. Chikenji
    Frontiers in Pharmacology, 12, 739510, 739510, Frontiers Media SA, 06 Sep. 2021, [Peer-reviewed], [Invited], [Last author, Corresponding author], [International Magazine]
    English, Scientific journal, Skeletal muscle undergoes vigorous tissue remodeling after injury. However, aging, chronic inflammatory diseases, sarcopenia, and neuromuscular disorders cause muscle loss and degeneration, resulting in muscular dysfunction. Cellular senescence, a state of irreversible cell cycle arrest, acts during normal embryonic development and remodeling after tissue damage; when these processes are complete, the senescent cells are eliminated. However, the accumulation of senescent cells is a hallmark of aging tissues or pathological contexts and may lead to progressive tissue degeneration. The mechanisms responsible for the effects of senescent cells have not been fully elucidated. Here, we review current knowledge about the beneficial and detrimental effects of senescent cells in tissue repair, regeneration, aging, and age-related disease, especially in skeletal muscle. We also discuss how senescence of muscle stem cells and muscle-resident fibro-adipogenic progenitors affects muscle pathologies or regeneration, and consider the possibility that immunosenescence leads to muscle pathogenesis. Finally, we explore senotherapy, the therapeutic targeting of senescence to treat age-related disease, from the standpoint of improving muscle regeneration.
  • Author Correction: Umbilical cord extracts improve osteoporotic abnormalities of bone marrow-derived mesenchymal stem cells and promote their therapeutic effects on ovariectomised rats (Scientific Reports, (2018), 8, 1, (1161), 10.1038/s41598-018-19516-6)
    Akira Saito, Kanna Nagaishi, Kousuke Iba, Yuka Mizue, Takako Chikenji, Miho Otani, Masako Nakano, Kazusa Oyama, Toshihiko Yamashita, Mineko Fujimiya
    Scientific Reports, 10, 1, Nature Research, 01 Dec. 2020
    English, Scientific journal
  • An enriched environment prevents cognitive impairment in an Alzheimer’s disease model by enhancing the secretion of exosomal microRNA-146a from the choroid plexus
    Masako Nakano, Kenta Kubota, Shin Hashizume, Eiji Kobayashi, Takako S. Chikenji, Yuki Saito, Mineko Fujimiya
    Brain, Behavior, & Immunity - Health, 9, 100149, 100149, Elsevier BV, Dec. 2020
    Scientific journal
  • Eccentric resistance training ameliorates muscle weakness in a mouse model of idiopathic inflammatory myopathies.
    Koichi Himori, Yuki Ashida, Daisuke Tatebayashi, Masami Abe, Yuki Saito, Takako Chikenji, Håkan Westerblad, Daniel C Andersson, Takashi Yamada
    Arthritis & rheumatology (Hoboken, N.J.), 73, 5, 848, 857, 15 Nov. 2020, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal, OBJECTIVE: High-force eccentric contractions (ECCs) have traditionally been excluded from rehabilitation programs of patients with idiopathic inflammatory myopathies (IIMs) due to unverified fear of causing muscle damage and inflammation. Here, we used an IIM animal model, experimental autoimmune myositis (EAM) mice, to investigated whether ECC training can be safely and effectively used to counteract muscle weakness in IIM. METHODS: EAM was induced in Balb/c mice by immunization with three injections of myosin emulsified in complete Freund's adjuvant. Control (CNT: n=12) and EAM (n=12) mice were exposed to an acute bout of 100 ECCs or 4 weeks of ECC training (20 ECCs every other day). To induce ECCs, plantar flexor muscles were electrically stimulated while the ankle was forcibly dorsiflexed. RESULTS: Less cell damage, as assessed by Evans blue dye uptake, was observed in EAM than in CNT muscles after an acute bout of 100 ECCs (P < 0.05). Maximum Ca2+ -activated force was decreased in skinned gastrocnemius muscle fibers from EAM mice and this was accompanied by increased expression of the endoplasmic reticulum (ER) stress proteins glucose-regulated protein 78 and 94 (P < 0.05). ECC training prevented the force decrease and the increase in ER stress proteins, and also enhanced the expression and myofibrillar binding of small heat shock proteins (sHSP) (P < 0.05), which can stabilize myofibrillar structure and function. CONCLUSION: ECC training protected against the reduction in myofibrillar force generating capacity in an IIM mouse model and this occurred via inhibition of ER stress responses and sHSP-mediated myofibrillar stabilization.
  • Bone marrow-derived mesenchymal stem cells improve cognitive impairment in an Alzheimer's disease model by increasing the expression of microRNA-146a in hippocampus.
    Masako Nakano, Kenta Kubota, Eiji Kobayashi, Takako S Chikenji, Yuki Saito, Naoto Konari, Mineko Fujimiya
    Scientific reports, 10, 1, 10772, 10772, 01 Jul. 2020, [Peer-reviewed], [International Magazine]
    English, Scientific journal, Alzheimer's disease (AD) is characterized by the accumulation of amyloid-β and tau. We previously reported that administration of bone marrow mesenchymal stem cells (BM-MSCs) ameliorates diabetes-induced cognitive impairment by transferring exosomes derived from these cells into astrocytes. Here, we show that intracerebroventricularly injected BM-MSCs improve cognitive impairment in AD model mice by ameliorating astrocytic inflammation as well as synaptogenesis. Although AD model mice showed an increase in NF-κB in the hippocampus, BM-MSC-treated AD model mice did not show this increase but showed an increase in levels of microRNA (miR)-146a in the hippocampus. Intracerebroventricularly injected BM-MSCs were attached to the choroid plexus in the lateral ventricle, and thus, BM-MSCs may secrete exosomes into the cerebrospinal fluid. In vitro experiments showed that exosomal miR-146a secreted from BM-MSCs was taken up into astrocytes, and an increased level of miR-146a and a decreased level of NF-κB were observed in astrocytes. Astrocytes are key cells for the formation of synapses, and thus, restoration of astrocytic function may have led to synaptogenesis and correction of cognitive impairment. The present study indicates that exosomal transfer of miR-146a is involved in the correction of cognitive impairment in AD model mice.
  • Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors
    Yuki Saito, Takako S. Chikenji, Takashi Matsumura, Masako Nakano, Mineko Fujimiya
    Nature Communications, Feb. 2020, [Peer-reviewed], [Corresponding author], [International Magazine]
    Scientific journal
  • Can an insole for obese individuals maintain the arch of the foot against repeated hyper loading?
    Yuki Saito, Takako S. Chikenji, Yuichi Takata, Tomoaki Kamiya, Eiichi Uchiyama
    BMC Musculoskeletal Disorders, Dec. 2019, [Peer-reviewed], [International Magazine]
    Scientific journal
  • p16INK4A-expressing mesenchymal stromal cells restore the senescence–clearance–regeneration sequence that is impaired in chronic muscle inflammation
    Takako S. Chikenji, Yuki Saito, Naoto Konari, Masako Nakano, Yuka Mizue, Miho Otani, Mineko Fujimiya
    EBioMedicine, 44, 86, 97, Elsevier {BV}, Jun. 2019, [Peer-reviewed], [Lead author, Corresponding author], [International Magazine]
    Scientific journal
  • Phosphorylated Platelet-Derived Growth Factor Receptor-Positive Cells With Anti-apoptotic Properties Accumulate in the Synovium of Patients With Rheumatoid Arthritis
    Takashi Matsumura, Yuki Saito, Tomoyuki Suzuki, Atsushi Teramoto, Yasuhiro Ozasa, Toshihiko Yamashita, Mineko Fujimiya, Takako S. Chikenji
    Frontiers in Immunology, 10, 241, Frontiers Media {SA}, Feb. 2019, [Peer-reviewed], [Last author, Corresponding author], [International Magazine]
    Scientific journal
  • Umbilical cord extracts improve osteoporotic abnormalities of bone marrow-derived mesenchymal stem cells and promote their therapeutic effects on ovariectomised rats
    Akira Saito, Kanna Nagaishi, Kousuke Iba, Yuka Mizue, Takako Chikenji, Miho Otani, Masako Nakano, Kazusa Oyama, Toshihiko Yamashita, Mineko Fujimiya
    Scientific Reports, 8, 1, Nature Publishing Group, 01 Dec. 2018, [Peer-reviewed], [International Magazine]
    English, Scientific journal
  • 作業療法疾患別ガイドライン 認知症　　　　　　　　　　　　　　　
    竹原 敦, 小川 敬之, 上城 憲司, 高木 雅之, 田平 隆行, 千見寺 貴子, 西浦 裕子, 西田 征治, 安田 大典, 山口 智晴, 磯 ふみ子, 市川 誠, 井上 忠俊, 木下 遥, 高坂 駿, 越當 美智子, 近藤 真知子, 坂上 真理, 坂本 千晶, 渋谷 晋太郎, 下田 佳央莉, 菅沼 一平, 仙波 梨沙, 田中 純子, 爲近 岳夫, 土谷 里織, 新中 浩司, 藤岡 崇, 古井 香苗, 松尾 崇史, 松尾 涼太, 村井 達彦, 山田 真季, 米澤 武人
    作業療法, 37, 1, 3, 11, (一社)日本作業療法士協会, Feb. 2018
    Japanese, Scientific journal
  • Activated forms of astrocytes with higher GLT-1 expression are associated with cognitive normal subjects with Alzheimer pathology in human brain.
    Eiji Kobayashi, Masako Nakano, Kenta Kubota, Nobuaki Himuro, Shougo Mizoguchi, Takako Chikenji, Miho Otani, Yuka Mizue, Kanna Nagaishi, Mineko Fujimiya
    Scientific reports, 8, 1, 1712, 1712, Springer Nature, 26 Jan. 2018, [Peer-reviewed], [International Magazine]
    English, Scientific journal, Although the cognitive impairment in Alzheimer's disease (AD) is believed to be caused by amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs), several postmortem studies have reported cognitive normal subjects with AD brain pathology. As the mechanism underlying these discrepancies has not been clarified, we focused the neuroprotective role of astrocytes. After examining 47 donated brains, we classified brains into 3 groups, no AD pathology with no dementia (N-N), AD pathology with no dementia (AD-N), and AD pathology with dementia (AD-D), which represented 41%, 21%, and 38% of brains, respectively. No differences were found in the accumulation of Aβ plaques or NFTs in the entorhinal cortex (EC) between AD-N and AD-D. Number of neurons and synaptic density were increased in AD-N compared to those in AD-D. The astrocytes in AD-N possessed longer or thicker processes, while those in AD-D possessed shorter or thinner processes in layer I/II of the EC. Astrocytes in all layers of the EC in AD-N showed enhanced GLT-1 expression in comparison to those in AD-D. Therefore these activated forms of astrocytes with increased GLT-1 expression may exert beneficial roles in preserving cognitive function, even in the presence of Aβ and NFTs.
  • An enriched environment prevents diabetes-induced cognitive impairment in rats by enhancing exosomal miR-146a secretion from endogenous bone marrow-derived mesenchymal stem cells.
    Kenta Kubota, Masako Nakano, Eiji Kobayashi, Yuka Mizue, Takako Chikenji, Miho Otani, Kanna Nagaishi, Mineko Fujimiya
    PloS one, 13, 9, e0204252, 2018, [Peer-reviewed], [International Magazine]
    English, Increasing evidence suggests that an enriched environment (EE) ameliorates cognitive impairment by promoting repair of brain damage. However, the mechanisms by which this occurs have not been determined. To address this issue, we investigated whether an EE enhanced the capability of endogenous bone marrow-derived mesenchymal stem/stromal cells (BM-MSCs) to prevent hippocampal damage due to diabetes by focusing on miRNA carried in BM-MSC-derived exosomes. In diabetic streptozotocin (STZ) rats housed in an EE (STZ/EE), cognitive impairment was significantly reduced, and both neuronal and astroglial damage in the hippocampus was alleviated compared with STZ rats housed in conventional cages (STZ/CC). BM-MSCs isolated from STZ/CC rats had functional and morphological abnormalities that were not detected in STZ/EE BM-MSCs. The miR-146a levels in exosomes in conditioned medium of cultured BM-MSCs and serum from STZ/CC rats were decreased compared with non-diabetic rats, and the level was restored in STZ/EE rats. Thus, the data suggest that increased levels of miR-146a in sera were derived from endogenous BM-MSCs in STZ/EE rats. To examine the possibility that increased miR-146a in serum may exert anti-inflammatory effects on astrocytes in diabetic rats, astrocytes transfected with miR-146a were stimulated with advanced glycation end products (AGEs) to mimic diabetic conditions. The expression of IRAK1, NF-κB, and tumor necrosis factor-α was significantly higher in AGE-stimulated astrocytes, and these factors were decreased in miR-146a-transfected astrocytes. These results suggested that EEs stimulate up-regulation of exosomal miR-146a secretion by endogenous BM-MSCs, which exerts anti-inflammatory effects on damaged astrocytes and prevents diabetes-induced cognitive impairment.
  • PDGFR Signaling Mediates Hyperproliferation and Fibrotic Responses of Subsynovial Connective Tissue Cells in Idiopathic Carpal Tunnel Syndrome
    Yuki Saito, Takako Chikenji, Yasuhiro Ozasa, Mineko Fujimiya, Toshihiko Yamashita, Anne Gingery, Kousuke Iba
    Scientific Reports, 7, 1, Springer Nature, Dec. 2017, [Peer-reviewed], [Corresponding author], ［Internationally co-authored］, [International Magazine]
    Scientific journal
  • Umbilical cord extracts improve diabetic abnormalities in bone marrow-derived mesenchymal stem cells and increase their therapeutic effects on diabetic nephropathy
    Kanna Nagaishi, Yuka Mizue, Takako Chikenji, Miho Otani, Masako Nakano, Yusaku Saijo, Hikaru Tsuchida, Shinichi Ishioka, Akira Nishikawa, Tsuyoshi Saito, Mineko Fujimiya
    SCIENTIFIC REPORTS, 7, 1, Aug. 2017, [Peer-reviewed], [International Magazine]
    English, Scientific journal
  • 多発性筋炎モデルマウスにおける骨格筋間葉系前駆細胞の異常性と運動刺激が与える影響
    齋藤 悠城, 千見寺 貴子, 松村 崇史, 水江 由佳, 藤宮 峯子
    理学療法学Supplement, 2016, 455, 455, 公益社団法人 日本理学療法士協会, 2017
    Japanese,

    【はじめに，目的】

    多発性筋炎に対する運動は炎症の助長や異所性組織を形成させるリスクがある。本研究では，骨格筋の炎症と再生，異所性組織形成において中心的な役割を果たす骨格筋間葉系前駆細胞（Mesenchymal Progenitor Cell：MPC）を中心として，運動刺激と炎症の助長および異所性組織形成のメカニズムを解明する。

    【方法】

    8週齢のBalb/cマウス（メス）に精製したBalb/c由来ミオシンと完全フロイトアジュバントをリンパ節付近に免疫し実験的自己免疫性筋炎（Experimental Autoimmune Myositis：EAM）を作成した。免疫後5週の時点で運動介入（17m/min，-20度傾斜，30分）を実施し，24時間後に腓腹筋を採取した。MPCはLineage陰性α7-integrin陰性PDGFRα陽性の細胞を単離した。単離後のMPCにて遺伝子発現解析（筋再生関連遺伝子Follistatin，IGF-1；抗炎症関連遺伝子TSG-6，IL-1Ra，IL-33；細胞周期阻害遺伝子p16ink4a；線維化関連遺伝子αSMA，TGFβ）を実施した。Control（Con）群，Controlに運動介入をしたControl-Exercise（Con-Ex）群，EAM群，EAMに運動介入をしたEAM-Exercise（EAM-Ex）群の4群で比較検討した。

    【結果】

    片側腓腹筋あたりのMPC細胞数はCon群（mean，0.37*105 cells；95% CI，0.24-0.50）と比較してEAM群（mean，2.02 *105 cells；95% CI，1.58-2.46）で有意に増加した（P＜0.001）。Con群ではEx介入によってMPC細胞数は有意に増加したが（mean，0.70 *105 cells；95% CI，0.56-0.84；P=0.02），EAM群ではEx介入で細胞数に有意差はなかった（mean，1.52 *105 cells；95% CI，1.90-1.14；P=0.132）。MPCの遺伝子発現解析の結果，Con-Ex群では筋再生関連，抗炎症関連および細胞周期阻害遺伝子の発現量増加を認めたが（P＜0.05），EAM-Ex群減少（P＜0.05），もしくは変化しなかった。さらに，EAM-Ex群では線維化関連遺伝子の発現が増加した（P＜0.05）。

    【結論】

    正常マウスと筋炎マウスのMPCでは運動刺激に対する反応が異なることを明らかにした。慢性炎症状態の骨格筋に対する運動刺激は，本来MPCがもつ抗炎症能力や筋サテライト細胞ニッチとしての働きを減弱させること，MPCにおけるαSMAやTGFβの発現が亢進させて骨格筋線維化の原因となる可能性を示唆した。また，間葉系細胞におけるp16ink4aの発現低下は様々な組織における線維化や再生不良に寄与することが報告されている。今回，筋炎モデルでは運動介入によってp16ink4a発現低下を認め，正常モデルでは発現亢進した。以上より，p16ink4aは適切な運動刺激のバイオマーカーとなるかもしれない。

  • Mesenchymal stem cell therapy ameliorates diabetic nephropathy via the paracrine effect of renal trophic factors including exosomes
    Kanna Nagaishi, Yuka Mizue, Takako Chikenji, Miho Otani, Masako Nakano, Naoto Konari, Mineko Fujimiya
    SCIENTIFIC REPORTS, 6, Oct. 2016, [Peer-reviewed], [International Magazine]
    English, Scientific journal
  • Bone marrow-derived mesenchymal stem cells improve diabetes-induced cognitive impairment by exosome transfer into damaged neurons and astrocytes
    Masako Nakano, Kanna Nagaishi, Naoto Konari, Yuki Saito, Takako Chikenji, Yuka Mizue, Mineko Fujimiya
    Scientific Reports, 6, 1, Springer Science and Business Media {LLC}, Apr. 2016, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
    Scientific journal
  • Transforming Growth Factor-beta (TGF-beta) Expression Is Increased in the Subsynovial Connective Tissue in a Rabbit Model of Carpal Tunnel Syndrome
    Takako Chikenji, Anne Gingery, Chunfeng Zhao, Matthias Vanhees, Tamami Moriya, Ramona Reisdorf, Kai-Nan An, Peter C. Amadio
    PLOS ONE, 9, 9, e108312, Sep. 2014, [Peer-reviewed], [Lead author], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal
  • Transforming Growth Factor-beta (TGF-beta) Expression Is Increased in the Subsynovial Connective Tissues of Patients With Idiopathic Carpal Tunnel Syndrome
    Takako Chikenji, Anne Gingery, Chunfeng Zhao, Sandra M. Passe, Yasuhiro Ozasa, Dirk Larson, Kai-Nan An, Peter C. Amadio
    JOURNAL OF ORTHOPAEDIC RESEARCH, 32, 1, 116, 122, Jan. 2014, [Peer-reviewed], [Lead author], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal
  • Delayed fracture healing in tetranectin-deficient mice
    Kousuke Iba, Yasuhisa Abe, Takako Chikenji, Kumiko Kanaya, Hironori Chiba, Koichi Sasaki, Takayuki Dohke, Takuro Wada, Toshihiko Yamashita
    JOURNAL OF BONE AND MINERAL METABOLISM, 31, 4, 399, 408, Jul. 2013, [Peer-reviewed], [International Magazine]
    English, Scientific journal
  • The effect of time after shear injury on the subsynovial connective tissue and median nerve within the rabbit carpal tunnel.
    Vanhees M, Chikenji T, Thoreson AR, Zhao C, Schmelzer JD, Low PA, An KN, Amadio PC
    Hand (New York, N.Y.), 8, 1, 54, 59, 1, Mar. 2013, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
  • The effect of lubricin on the gliding resistance of mouse intrasynovial tendon.
    Hayashi M, Zhao C, Thoreson AR, Chikenji T, Jay GD, An KN, Amadio PC
    PloS one, 8, 12, e83836, 12, 2013, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
  • Skeletal muscle and bone marrow derived stromal cells: A comparison of tenocyte differentiation capabilities
    Adam A. Sassoon, Yasuhiro Ozasa, Takako Chikenji, Yu-Long Sun, Dirk R. Larson, Mary L. Maas, Chunfeng Zhao, Jin Jen, Peter C. Amadio
    JOURNAL OF ORTHOPAEDIC RESEARCH, 30, 11, 1710, 1718, Nov. 2012, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal
  • Subsynovial connective tissue is sensitive to surgical interventions in a rabbit model of carpal tunnel syndrome
    Yu-Long Sun, Tamami Moriya, Chunfeng Zhao, Ramona L. Kirk, Takako Chikenji, Sandra M. Passe, Kai-Nan An, Peter C. Amadio
    JOURNAL OF ORTHOPAEDIC RESEARCH, 30, 4, 649, 654, Apr. 2012, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal
  • Comparison of Different Fixation Methods of the Suture-Button Implant for Tibiofibular Syndesmosis Injuries
    Atsushi Teramoto, Daisuke Suzuki, Tomoaki Kamiya, Takako Chikenji, Kota Watanabe, Toshihiko Yamashita
    AMERICAN JOURNAL OF SPORTS MEDICINE, 39, 10, 2226, 2232, Oct. 2011, [Peer-reviewed], [International Magazine]
    English, Scientific journal
  • Wrist Positioning and Muscle Activities in the Wrist Extensor and Flexor During Piano Playing
    Naoki Oikawa, Sadako Tsubota, Takako Chikenji, Gyoku Chin, Mitsuhiro Aoki
    HONG KONG JOURNAL OF OCCUPATIONAL THERAPY, 21, 1, 41, 46, Jun. 2011, [Peer-reviewed], [International Magazine]
    English, Scientific journal
  • Effects of different temperatures, velocities and loads on the gliding resistance of flexor digitorum profundus tendons in a human cadaver model
    Tamami Moriya, Takako Chikenji, Andrew R. Thoreson, Chunfeng Zhao, Kai-Nan An, Peter C. Amadio
    JOURNAL OF BIOMECHANICS, 44, 7, 1414, 1416, Apr. 2011, [Peer-reviewed], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal
  • Distribution of Nerve Endings in Human Distal Interphalangeal Joint and Surrounding Structures
    Takako Chikenji, Richard A. Berger, Mineko Fujimiya, Daisuke Suzuki, Sadako Tsubota, Kai-Nan An
    JOURNAL OF HAND SURGERY-AMERICAN VOLUME, 36A, 3, 406, 412, Mar. 2011, [Peer-reviewed], [Lead author], ［Internationally co-authored］, [International Magazine]
    English, Scientific journal
  • Distribution of Nerve Endings in the Human Proximal Interphalangeal Joint and Surrounding Structures
    Takako Chikenji, Daisuke Suzuki, Mineko Fujimiya, Tamami Moriya, Sadako Tsubota
    JOURNAL OF HAND SURGERY-AMERICAN VOLUME, 35A, 8, 1286, 1293, Aug. 2010, [Peer-reviewed], [Lead author, Corresponding author], [International Magazine]
    English, Scientific journal
  • A comparison of the strength of the abduction of the little and index fingers and palmar abduction and opposition of the thumb between college baseball players and inexperienced sports players
    Takako Chikenji, Hajime Toda, Chin Gyoku, Naoki Oikawa, Masaki Katayose, Sadako Tsubota
    Journal of Musculoskeletal Research, 13, 2, 75, 82, Jun. 2010, [Peer-reviewed], [Lead author, Corresponding author], [International Magazine]
    English, Scientific journal

Other Activities and Achievements

Lectures, oral presentations, etc.

  • 老化細胞の免疫回避機構に着眼したエリテマトーデスの皮膚病態の解明　　　　　　　　　　　　　　　
    山本 瀬菜, 齋藤 悠城, 中野 世那, 佐藤 吏紗, 三浦 倫寛, 長岡賢太郎, 北 愛里紗, 宮島 真貴, 井嶋 翔吾, 谷口 浩二, 新井田厚司, 千見寺貴子
    日本薬理学会第145年会, 28 Mar. 2025
  • 細胞老化システムから探る骨格筋の再生・変性メカニズム　　　　　　　　　　　　　　　
    千見寺貴子, 齋藤悠城
    細胞老化システムから探る骨格筋の再生・変性メカニズム, 21 Mar. 2025, Nominated symposium
    [Invited]
  • Cell senescence and inflammation.　　　　　　　　　　　　　　　
    Chikenji T.
    Sakura Science Program Inauguration & IJSSTE (Hokkaido) Science Seminar, 10 Dec. 2024, Invited oral presentation
    [Invited]
  • 細胞老化が組織恒常性と慢性炎症性疾患に及ぼす影響　　　　　　　　　　　　　　　
    千見寺貴子, 齋藤悠城
    第47回日本分子生物学会年会, 27 Nov. 2024, Public symposium
    [Invited]
  • OTのエビデンス構築へ向けたサイエンス最前線　　　　　　　　　　　　　　　
    千見寺貴子
    第12回起業・経営OTサミット, 09 Nov. 2024, Invited oral presentation
    [Invited]
  • 老化細胞の免疫回避機構に着眼したエリテマトーデスの皮膚病態の解明　　　　　　　　　　　　　　　
    山本 瀬菜, 齋藤 悠城, 中野 世那, 佐藤 吏紗, 三浦 倫寛, 長岡 賢太郎, 北 愛里紗, 宮島 真貴, 井嶋 翔吾, 谷口 浩二, 新井田 厚司, 千見寺 貴子
    第97回日本生化学大会, 06 Nov. 2024, Oral presentation
  • 自己免疫疾患における細胞老化と細胞間ネットワーク　　　　　　　　　　　　　　　
    千見寺貴子, 齋藤悠城
    第97回日本生化学大会, 06 Nov. 2024, Public symposium
    [Invited]
  • Understanding stress from animal models: Insight for occupational therapy　　　　　　　　　　　　　　　
    Chikenji T.
    International Symposium “Loneliness, Isolation, and Diversity: Pursuing Justice through Occupational Therapy and Occupational Science, 04 Nov. 2024, Invited oral presentation
    [Invited]
  • Effects of mechanical stress and hyperglycemia on senescence in skeletal muscle　　　　　　　　　　　　　　　
    Kasseki D., Saito Y., Yamamoto S., Chikenji TS
    12th annual meeting of the international cytokine & interferon society jointly Korean association of immunologists international meeting 2024, 21 Oct. 2024, Poster presentation
  • Identification of TGFB1-upregulated senescent fibroblasts in keloids　　　　　　　　　　　　　　　
    Yamamoto K., Yamamoto S., Kita A., Ueda N., Yotsuyanagi T., Saito Y., Chikenji TS
    12th annual meeting of the international cytokine & interferon society jointly Korean association of immunologists international meeting 2024, 21 Oct. 2024, Poster presentation
  • Senescent neural progenitor cells increased neurite outgrowth in mouse model of autism spectrum disorders　　　　　　　　　　　　　　　
    Miyajima M., Saito Y., Sato T., Yamamoto S., Tomaru U., Ishizu A., Chikenji TS
    12th annual meeting of the international cytokine & interferon society jointly Korean association of immunologists international meeting 2024, 21 Oct. 2024, Poster presentation
  • Characterization of healer-specific senescent fibroblasts in diabetic foot ulcer by single-cell RNA-seq analysis　　　　　　　　　　　　　　　
    Ueda N., Saito Y., Yamamoto S., Kita A., Yotsuyanagi T., Chikenji TS
    12th annual meeting of the international cytokine & interferon society jointly Korean association of immunologists international meeting 2024, 21 Oct. 2024, Poster presentation
  • Cellular Senescence in the hippocampus regulates resilience to chronic stress by secreting neurogenic/protective factors.　　　　　　　　　　　　　　　
    Sato T., Saito Y., Yamamoto S., Miura N., Miyajima M., Chikenji TS
    12th annual meeting of the international cytokine & interferon society jointly Korean association of immunologists international meeting 2024, 21 Oct. 2024, Poster presentation
  • HLA class I-downregulated senescent epidermal basal cells orchestrate skin pathology in systemic lupus erythematosus.　　　　　　　　　　　　　　　
    Yamamoto S., Saito Y., Nakano S., Sato T., Miura N., Nagaoka K., Kita A., Miyajima M., Ijima D., Taniguchi K., Niida A., Chikenji TS
    12th annual meeting of the international cytokine & interferon society jointly Korean association of immunologists international meeting 2024, 21 Oct. 2024, Oral presentation
  • Diverse roles of cellular senescence in skeletal muscle inflammation and regeneration.　　　　　　　　　　　　　　　
    Saito Y., Chikenji T.
    Joint Conference of the 22nd Annual Meeting of Asian and Oceanian Myology Center and the 10th Annual Meeting of Japan Muscle Society (AOMC-JMS 2024), 12 Sep. 2024, Invited oral presentation
    [Invited]
  • ケロイドで増加するTGFB1を高発現する老化線維芽細胞のシングルセルRNA-seq解析による同定　　　　　　　　　　　　　　　
    山本 花練, 山本 瀬菜, 北 愛里紗, 齋藤 悠城, 千見寺貴子
    第45回 日本炎症再生医学会, 17 Jul. 2024, Poster presentation
  • 細胞老化随伴分泌現象は全身性エリテマトーデスにおける表皮細胞の免疫原性を高める　　　　　　　　　　　　　　　
    山本 瀬菜, 齋藤 悠城, 中野 世那, 佐藤 吏紗, 三浦 倫寛, 長岡賢太郎, 北 愛里紗, 宮島 真貴, 井嶋 翔吾, 谷口 浩二, 新井田厚司, 千見寺貴子
    第45回 日本炎症再生医学会, 17 Jul. 2024, Poster presentation
  • Cellular senescence of synovial fibroblasts in rheumatoid arthritis model mice　　　　　　　　　　　　　　　
    Taiki Iwamoto, Yuki Saito, Sena Yamamoto, Kentaro Nagaoka, Yasutaka Murahashi, Atsushi Teramoto, Kosuke Iba, Toshihiko Yamashita, Takako Chikenji
    An ASCB|EMBO meeting Cell Bio 2023, 04 Dec. 2023, English, Poster presentation
  • Cellular Senescence in Epidermal Stem Cells as a Potential Driver of Lupus Erythematosus Skin Lesions　　　　　　　　　　　　　　　
    Sena Yamamoto, Yuki Saito, Tsukasa Sato, Norihiro Miura, Kentaro Nagaoka, Taiki Iwamoto, Maki Miyajima, Arisa Kita, Takako S. Chikenji
    An ASCB|EMBO meeting Cell Bio 2023, 04 Dec. 2023, English, Poster presentation
  • Exercise-induced senescence-like gene signature in fibro/adipogenic progenitors is impaired in diabetes muscle　　　　　　　　　　　　　　　
    Yuki Saito, Norihiro Miura, Sena Yamamoto, Tsukasa Sato, Kentaro Nagaoka, Taiki Iwamoto, Maki Miyajima, Arisa Kita, Takako S. Chikenji
    An ASCB|EMBO meeting Cell Bio 2023, 03 Dec. 2023, English, Nominated symposium
  • Involvement of Cellular Senescence in the Pathogenesis of Lupus Nephritis in Mice　　　　　　　　　　　　　　　
    Kentaro Nagaoka, Yuki Saito, Shogo Ijima, Sena Yamamoto, Tsukasa Sato, Norihiro Miura, Taiki Iwamoto, Maki Miyajima, Takako S. Chikenji
    An ASCB|EMBO meeting Cell Bio 2023, 02 Dec. 2023, English, Poster presentation
  • Identification of TGFB1-upregulated senescent fibroblasts in keloids　　　　　　　　　　　　　　　
    Karen Yamamoto, Sena Yamamoto, Arisa Kita, Yuki Saito, Takako Chikenji
    5th FHS International Conference, 20 Oct. 2023, English, Poster presentation
  • 自閉スペクトラム症モデルマウスにおける神経前駆細胞の細胞老化　　　　　　　　　　　　　　　
    宮島真貴, 齋藤悠城, 佐藤吏紗, 山本瀬菜, 三浦倫寛, 千見寺貴子
    第44回日本炎症・再生医学会, 12 Jul. 2023, Poster presentation
  • 全身性エリテマトーデス皮膚炎における老化細胞の役割とシングルセル解析による病態解明　　　　　　　　　　　　　　　
    山本瀬菜, 齋藤悠城, 井嶋翔吾, 北愛里紗, 三浦倫寛, 佐藤吏紗, 宮島真貴, 千見寺貴子
    第44回日本炎症・再生医学会, 12 Jul. 2023, Poster presentation
  • 滑膜線維芽細胞の細胞老化は関節リウマチにおける炎症性組織プライミング誘導に関与する　　　　　　　　　　　　　　　
    齋藤悠城, 岩本大輝, 山本瀬菜, 宮島真貴, 村橋靖崇, 寺本篤史, 射場浩介, 山下敏彦, 千見寺貴子
    第44回日本炎症・再生医学会, 12 Jul. 2023, Poster presentation
  • 組織再生とリハビリテーション〜基礎から臨床へのトランスレーショナル研究〜　　　　　　　　　　　　　　　
    千見寺貴子
    第53回北海道作業療法学会学術大会, 23 Jun. 2023, Keynote oral presentation
    [Invited]
  • Fisetin improved depressive behavior in murine lupus by decreasing senescent neural cell.　　　　　　　　　　　　　　　
    Yuki Saito, Maki Miyajima, Sena Yamamoto, Tsukasa Sato, Norihiro Miura, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, English, Nominated symposium
  • Diabetic wound impaired injury-induced transient senescence in adipose tissue that promotes the normal wound healing process.　　　　　　　　　　　　　　　
    Arisa Kita, Yuki Saito, Norihiro Miura, Sena Yamamoto, Tsukasa Sato, Takatoshi Yotsuyanagi, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, English, Poster presentation
  • Dual role of TGF-β1 in cellular senescence of tubular cells and hyper-proliferation of fibroblasts to aggravate lupus nephritis.　　　　　　　　　　　　　　　
    Shogo Ijima, Yuki Saito, Maki Miyajima, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, English, Poster presentation
  • Altered regulation of senescence-associated secretory phenotype in hippocampus modulates resilience to chronic mild psychiatric stress.　　　　　　　　　　　　　　　
    Tsukasa Sato, Yuki Saito, Maki Miyajima, Sena Yamamoto, Norihiro Miura, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, English, Poster presentation
  • Lower-expression of Cdkn2a is associated with dysregulation of fibro-adipogenic progenitors results in skeletal muscle atrophy and degeneration in diabetic mice.　　　　　　　　　　　　　　　
    Norihiro Miura, Yuki Saito, Arisa Kita, Maki Miyajima, Tsukasa Sato, Sena Yamamoto, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, English, Poster presentation
  • Senolysis by fisetin ameliorates lupus erythematosus-like skin lesions in MRL/lpr mice.　　　　　　　　　　　　　　　
    Sena Yamamoto, Yuki Saito, Shogo Ijima, Arisa Kita, Norihiro Miura, Tsukasa Sato, Maki Miyajima, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, English, Poster presentation
  • Accumulation of senescent neurons in mice model of autism spectrum disorder with abnormal synaptic pruning.　　　　　　　　　　　　　　　
    Maki Miyajima, Yuki Saito, Tsukasa Sato, Norihiro Miura, Sena Yamamoto, Mineko Fujimiya, Takako S. Chikenji
    The 6th International Cell Senescence Association Conference, Dec. 2021, Poster presentation
  • 〔Major achievements〕骨格筋再生プロセスにおける細胞老化　　　　　　　　　　　　　　　
    千見寺貴子, 齋藤悠城, 藤宮峯子
    第20回日本再生医療学会 シンポジウム11, Public symposium
    Mar. 2021, [Invited]
  • Exercise enhances skeletal muscle regeneration by promoting senescence in fibro-adipogenic progenitors　　　　　　　　　　　　　　　
    Yuki Saito, Takashi Matsumura, Mineko Fujimiya, Takako S. Chikenji
    米国整形外科基礎学会 Annual meeting of Orthopaedic Research Society, Feb. 2020, English, Oral presentation
  • Senescent Cells Escape From Immune Clearance In Fibrotic Subsynovial Connective Tissue In Carpal Tunnel Syndrome　　　　　　　　　　　　　　　
    Takako S. Chikenji, Yuki Saito, Alyssa Vrieze, Sandra Passe, Tamara Tchkonia, James L. Kirkland, Peter C. Amadio, Anne Gingery
    米国整形外科基礎学会 Annual meeting of Orthopaedic Research Society, Feb. 2020, English, Oral presentation
  • 細胞老化と健康寿命　　　　　　　　　　　　　　　
    千見寺貴子
    北海道大学保健科学研究院 公開講座, Nov. 2019, Japanese, Public discourse
    [Invited]
  • 細胞老化ークリアランスーリモデリング連鎖 に基づく新たな再生医療の可能性　　　　　　　　　　　　　　　
    千見寺貴子
    北海道移植免疫研究会, Sep. 2019, Japanese, Public discourse
    [Invited]
  • Role of platelet-derived growth factor (PDGF) signaling in synovial fibrosis.　　　　　　　　　　　　　　　
    Takako S. Chikenji
    FHS International conference, Jul. 2019, English, Nominated symposium
    [Invited]
  • Platelet-Derived Growth Factor Receptor Alpha Signaling in Carpal Tunnel Syndrome　　　　　　　　　　　　　　　
    Takako S. Chikenji
    Musculoskeletal Research Conference, Mayo Clinic, USA, Apr. 2019, English, Public discourse
    [Invited]
  • A Stimulation of Adult Mesenchymal Stromal Cell Promote Chronic Muscular Inflammation Healing in Multiple Myositis.　　　　　　　　　　　　　　　
    Chikenji T, Saito Y, Mizue Y, Fujimiya M
    Keystone Symposia Conference. Aging and Mechanisms of Aging-Related Disease., May 2017, English, Poster presentation
  • The Effects of Estradiol on Mesenchymal Stem Cells in Subsynovial Connective Tissue of Carpal Tunnel Syndrome In vitro.　　　　　　　　　　　　　　　
    Chikenji T, Saito Y, Ozasa Y, Fujimiya M, Yamashita T, Iba K
    Orthopedic Research Society 63th Annual Meeting., Mar. 2017, English, Poster presentation
  • 細胞療法に適した間葉系幹細胞の製造法の開発．　　　　　　　　　　　　　　　
    千見寺貴子
    第2回北海道ナノバイオ研究会(HNB)シンポジウム, Aug. 2016, Japanese, Nominated symposium
    [Invited]
  • Meet the Experience海外学会・研修体験ーグローバル化を目指してー　　　　　　　　　　　　　　　
    千見寺貴子
    日本ハンドセラピィ学会, Apr. 2016, Japanese, Nominated symposium
    [Invited]
  • Mesenchymal Stem Cells in Subsynovial Connective Tissue in Carpal Tunnel.　　　　　　　　　　　　　　　
    Chikenji T, Saito Y, Mizue Y, Nagaishi K, Fujimiya M, Yamashita T, Iba K
    Orthopedic Research Society 62th Annual Meeting., Mar. 2016, English, Poster presentation
  • Transforming growth factor-beta expression is increased in subsynovial connective tissues in human idiopathic carpal tunnel syndrome.　　　　　　　　　　　　　　　
    Chikenji, T, Gingery, A, Zhao, C, Passe, S, An, K, Amadio, PC
    Orthopedic Research Society 59th Annual Meeting., Feb. 2013, English, Poster presentation
  • A Comparison of the Strength of the Abduction of the Little and Index fingers and Palmar Abduction and Opposition of the Thumb Between College Baseball Players and Non-athletes.　　　　　　　　　　　　　　　
    Chikenji, T. Toda, H. Gyoku, C. Oikawa, N. Katayose, M. Ota, H, Tsubota, S
    The 9th Congress of Asian Pacific Federation of Societies for Surgery of the Hand and The 5th Congress of Asian Pacific Federation of Societies for Hand Therapist., Oct. 2012, English, Oral presentation
  • Absence of Myofibroblasts in Subsynovial Connective Tissues in Human and Rabbit Models of Carpal Tunnel Syndrome.　　　　　　　　　　　　　　　
    Chikenji, T. Vanhees, M. Moriya, T. Zhao, C. An, K-N, Amadio PC
    the 8th International Hand and Wrist Biomechanics Symposium., Apr. 2012, English, Public symposium
  • Fibroblast-Specific Protein 1 is Increased in Subsynovial Connective Tissues in Idiopathic Carpal Tunnel Syndrome.　　　　　　　　　　　　　　　
    Chikenji, T. Zhao, C. Ettema, A. Sun, Y-L. Hayashi, M, An, K-N, Amadio PC
    Orthopedic Research Society 58th Annual Meeting., Feb. 2012, English, Poster presentation
  • Absence of Myofibroblasts in Subsynovial Connective Tissues in Human and Rabbit Models of Carpal Tunnel Syndrome.　　　　　　　　　　　　　　　
    Chikenji, T. Vanhees, M. Moriya, T. Zhao, C. An, K-N, Amadio PC
    Orthopedic Research Society 58th Annual Meeting. San Francisco, Feb. 2012, English, Poster presentation
  • Distribution of Nerve Endings in Distal Interphalangeal Joint and Surrounding Structures.　　　　　　　　　　　　　　　
    Chikenji T, Berger RA, Fujimiya M, Suzuki D, An K-N, Tsubota S
    Orthopedic Research Society 57th Annual Meeting., Jan. 2011, English, Poster presentation
  • Distribution of Nerve Endings in Proximal Interphalangeal Joint and Surrounding Structures.　　　　　　　　　　　　　　　
    Chikenji T, Suzuki D, Fujimiya M, Moriya T, Kamiya T, Tsubota S
    Orthopedic Research Society 56th Annual Meeting, Mar. 2009, English, Oral presentation
  • Distribution of nerve fiber and mechanoreceptor in the metacarpophlangeal and proximal interphalangeal joints: a preliminary study.　　　　　　　　　　　　　　　
    Chikenji T, Suzuki D, Aoki M, Tsubota S, Tatsumi H
    7th Congress of Asian Pacific Federation of Societies for Surgery of the Hand., Feb. 2008, English, Oral presentation
  • A new rehabilitaion protocol for massive rotator cuff repair.　　　　　　　　　　　　　　　
    Chikenji, T. Kasai, T. Kubo, S. Mitani, M. Ogawa
    7th congress of the international federation of societies for hand therapy., Mar. 2007, English, Public symposium

Affiliated academic society

  • 日本ハンドセラピィ学会　　　　　　　　　　　　　　　
  • JAPANESE ASSOCIATION OF OCCUPATIONAL THERAPISTS　　　　　　　　　　　　　　　
  • JAPANESE SOCIETY FOR SURGERY OF THE HAND　　　　　　　　　　　　　　　
  • THE JAPANESE SOCIETY FOR REGENERATIVE MEDICINE　　　　　　　　　　　　　　　
  • International Cell Senescence Association　　　　　　　　　　　　　　　
  • Orthopedic Research Society　　　　　　　　　　　　　　　
  • 日本炎症再生学会　　　　　　　　　　　　　　　

Research Themes

  • Elucidating the Pathophysiology of Rheumatoid Arthritis and Strategies for Joint Regeneration through the Mechanisms of Senescent Cell Fate Determination
    KAKENHI
    Apr. 2024 - Mar. 2027
    千見寺 貴子, 齋藤悠城
    Japan Society for the Promotion of Science, 基盤研究(B), 北海道大学, 24K02561
  • Elucidating the Divergence between Healthy Aging and Age-Related Diseases through Senescent-Origin Cells
    KAKENHI
    Jun. 2023 - Mar. 2026
    千見寺 貴子, 齋藤 悠城
    Japan Society for the Promotion of Science, 挑戦的研究(萌芽), 北海道大学, 23K18443
  • Revealing the pathomechanisms of rheumatoid arthritis through exploring the intercellular networks woven by senescent cells　　　　　　　　　　　　　　　
    Jul. 2024 - 2026
    Japan Agency for Medical Research and Development (AMED), 24016820
  • Understanding Stress-Resilient Cell-Cell Communications through Cellular Senescence　　　　　　　　　　　　　　　
    Fusion Oriented Research for disruptive Science and Technology
    2023 - 2026
    千見寺貴子
    Japan Science and Technology Agency, JPMJFR225E
  • 老化細胞のメカノバイオロジー: メカニカルストレスによる細胞老化制御への挑戦　　　　　　　　　　　　　　　
    科学研究費助成事業 挑戦的研究(萌芽)
    Jun. 2022 - Mar. 2025
    齋藤 悠城, 千見寺 貴子
    日本学術振興会, 挑戦的研究(萌芽), 札幌医科大学, 22K19757
  • 糖尿病に伴うサルコペニア病態における老化細胞の役割の解明　　　　　　　　　　　　　　　
    2024 - 2025
    公益財団法人 中冨健康科学振興財団
  • 細胞老化制御に基づく組織再生リハビリテーション:セノリハビリテーションの基盤創成
    Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)
    Apr. 2021 - Mar. 2024
    齋藤 悠城 千見寺貴子
    老化細胞は安定的に細胞周期を停止する一方、代謝的には非常に活発で、サイトカインやケモカイン、エクソソームなど様々な生物活性を有する因子を分泌する。この分泌現象を老化関連分泌表現型(Senescence-associate secretory phenotype: SASP)と呼ぶ。このSASPによって、老化細胞は周囲の細胞に働きかけて組織を再生へ導く一方で、老化細胞の蓄積は組織の変性や慢性炎症を引き起こすことも知られている。これまでの研究でメカニカルストレスによって細胞老化を制御できる可能性を見い出してきたことから、リハビリテーションによる細胞老化を制御することで組織再生を促す、セノリハビリテーションという新しい治療アプローチの可能性を見出した。本年度は、老化細胞に特徴的なメカニカルストレスの感受性を明らかにするため、in vitroで老化細胞モデルを作成し、その遺伝子発現を解析した。老化細胞において、いくつかの細胞骨格やインテグリンなど、増殖細胞とは異なるいくつかの特徴を明らかにした。また、伸展培養装置を用い、細胞にメカニカルストレスを負荷することで、メカニカルストレスによる細胞老化誘導メカニズムの解明と誘導後の老化細胞の表現系解析を実施した。特定の強度で細胞老化が誘導されること、また慢性炎症状態を模擬した成長因子やサイトカインで刺激と共に、メカニカルストレスを負荷することで、異なる表現系の細胞老化が誘導されることもわかってきた。これらの研究を継続することで、セノリハビリテーションという細胞・分子レベルから細胞老化を制御する新たな治療基盤の創成を目指す。
    Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (B), Sapporo Medical University, 21H03293
  • 老化細胞ニッチを標的とした関節リウマチの制御と関節再生戦略の創成
    Grants-in-Aid for Scientific Research Grant-in-Aid for Scientific Research (B)
    Apr. 2021 - Mar. 2024
    齋藤 (千見寺) 貴子
    我々は, 関節リウマチ(Rheumatoid Arthritis; RA)の滑膜で、有害性老化細胞を中心とした微小環境「老化細胞ニッチ」の形成がRA滑膜炎の真の病態像である可能性に辿り着いた。本研究では、1) RA滑膜の老化細胞ニッチを解明する。ついで、2)老化細胞ニッチの破壊による滑膜炎制御法を確立し、炎症を抑えた滑膜に3)組織の再生を促すヘルパー老化細胞を誘導することで滑膜を“関節構造の再生の場”へと変容し、骨・軟骨の再生を促すことで構造的寛解を超えて再び機能する関節の獲得を目指す。
    まず、老化細胞ニッチの解明として、RA患者滑膜を採取し、組織学的解析により老化細胞の同定を行った。RA患者滑膜には複数の細胞老化因子を発現する細胞が存在し、周辺に増殖性の高い細胞の集積を認めている。次に、RA患者滑膜の細胞を滑膜組織由来のfibroblast like synoviocytes(FLS)を単離し、老化細胞と非老化細胞の共培養を実施し、老化細胞ニッチの表現形を解析している。In vitroにおいても、RA由来の老化細胞の周辺で増殖性の高い細胞が集積し、アポトーシス抵抗性、MMPなど関節破壊に関連する因子の上昇を認めている。次年度は、老化細胞ニッチ因子ならびにニッチ因子弱点を明らかにするため、老化細胞ニッチの網羅的解析を行うと同時に、候補に上げられたニッチ因子についてノックアウトを行い、細胞ニッチの形成が阻害されるか?老化細胞ニッチを形成する細胞の細胞死を誘導できるか？を検討する。次に、同定した老化細胞ニッチの弱点をもとに、FDA承認薬を用いてニッチ破壊薬の同定を行う。さらに、RAにおいて老化細胞ニッチが関節炎の発症と進行に関与するかを明らかにするため、FLS細胞に細胞老化を誘導し、老化細胞を野生型マウスの膝関節内に投与して、滑膜炎が誘導されるか検討する予定である。
    Japan Society for the Promotion of Science, Grant-in-Aid for Scientific Research (B), Hokkaido University, 21H03049
  • シングルセルRNA-seq解析による老化細 胞を中心とした関節リウマチの病態解明　　　　　　　　　　　　　　　
    2023 - 2024
    公益財団法人持田記念医学薬学振興財団
  • 糖尿病性腎症に対する間葉系幹細胞の臨床応用へ向けた品質管理と有効な評価マーカーの確立　　　　　　　　　　　　　　　
    札幌ライフサイエンス産業活性化事業／事業化支援補助金
    Apr. 2020 - Mar. 2021
    千見寺貴子
    ノーステック 財団, Hokkaido University, Principal investigator
  • Regulation of muscle stem cell and mesenchymal stem cell by exercise induced metabolic and mechanical stress
    Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists
    Apr. 2018 - Mar. 2021
    Saito Yuki
    Exercise activates muscular stem cells, mesenchymal stem cells (MSCs), and immune cells to promote muscle hypertrophy and anti-inflammatory effects, resulting in maintaining skeletal muscle homeostasis. On the other hand, excessive exercise can induce inflammation and fibrosis in chronic inflammatory myopathy patients. In this study, we clarified a part of the mechanism of skeletal muscle regeneration and fibrosis induced by exercise by animal experiment. Furthermore, in vitro cell culture studies revealed that myoblasts and skeletal muscle-derived fibroblasts altered their response to mechanical stress depending on the inflammatory state.These findings might be contribute the development of effective and safe treatments for chronic myopathy patients.
    Japan Society for the Promotion of Science, Grant-in-Aid for Early-Career Scientists, Sapporo Medical University, 18K17722
  • Cellular senescence system of carpal tunnel syndrome and development of novel therapeutic methods
    Grants-in-Aid for Scientific Research Grant-in-Aid for Early-Career Scientists
    Apr. 2018 - Mar. 2021
    Chikenji Takako
    Carpal tunnel syndrome (CTS) is the most common compression neuropathy. Effective treatments are limited to surgical interventions, and novel treatments have not yet been developed. In CTS patients, fibrosis of the subsynovial connective tissue surrounding the median nerve in the carpal tunnel is known as a pathological condition that compresses the median nerve in the carpal tunnel. In this study, we investigated cellular senescence in subsynovial connective tissue in CTS. In the CTS patients, PDGFRa + cells expressed both senescence factors and the macrophage checkpoint. PDGFRa + senescent cells avoided the phagocytosis of macrophages. Furthermore, PDGFRa+ senescent cells promoted the proliferation of adjacent fibroblasts. When senescent fibroblasts were transplanted into the carpal tunnel of a rabbit model, an increase in fibrosis-related genes was observed in the subsynovial connective tissue. Finally, one of senolytics induced apoptosis in PDGFRa + rather than control cells.
    Japan Society for the Promotion of Science, Grant-in-Aid for Early-Career Scientists, Sapporo Medical University, 18K16668
  • The role of muscle mesenchymal progenitors in exercise; double-edged sword of mesenchymal progenitors in muscular disease.
    Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)
    01 Apr. 2016 - 31 Mar. 2019
    Saito Yuki, Chikenji Takako, Fujimiya Mineko
    Exercise-induced damage triggers muscle regeneration by activating satellite cells, fibro-adipogenic progenitors (FAPs), and immune cells. FAPs facilitated by exercise play roles for muscle remodeling. On the other hand, in the pathological conditions such as chronic inflammatory myopathy (CIM), exercise-induced damage rather exacerbates the inflammation and fibrosis in the muscle. Although it is considered that FAPs are key regulator for muscle inflammation and fibrosis, the cellular mechanisms are not completely understood.
    Here we aimed to demonstrate the mechanism for different roles of exercise-induced damage between normal and CIM by focusing on cell senescence in FAPs. we found that both of sufficient senescence and up-regulation of p38 MAPK, a pro-apoptotic signal, might be necessary for exercise-induced muscle regeneration. On the other hand, insufficient senescence and up-regulation of NF-ΚB, a anti-apoptotic signal might cause exercise-induced inflammation and fibrosis.
    Japan Society for the Promotion of Science, Grant-in-Aid for Young Scientists (B), Sapporo Medical University, 16K16430
  • Do degenerated synovium with rheumatoid arthritis become scaffolds for abnormal synovial mesenchymal stem cells?
    Grants-in-Aid for Scientific Research Grant-in-Aid for Research Activity start-up
    26 Aug. 2016 - 31 Mar. 2018
    Matsumura Takashi, CHIKENJI Takako, SAITO Yuki, FUJIMIYA Mineko, OZASA Yasuhiro, SUZUKI Tomoyuki, TERAMOTO Atsushi, YAMASHITA Toshihiko
    Synovial tissue was collected from RA patient group, control group (knee ligament injury etc.), and immunohistological examination was conducted. Accumulation of phosphorylated platelet-derived growth factor receptor-αβ (pPDGFRαβ) positive FLS was observed in the synovial membrane of RA. Furthermore, the expression of Bcl-2 of apoptosis-resistant marker was elevated in pPDGFRαβ positive cells, p16 of cyclin-dependent kinase inhibitor was decreased. In RA synovium, it suggested that cell proliferation cannot be stopped, apoptosis is inhibited and cells might accumulate without apoptosis.
    Japan Society for the Promotion of Science, Grant-in-Aid for Research Activity start-up, Sapporo Medical University, 16H07096
  • The Effects of Estradiol on Mesenchymal Stem Cells in Subsynovial Connective Tissue of Carpal Tunnel Syndrome
    Grants-in-Aid for Scientific Research Grant-in-Aid for Young Scientists (B)
    01 Apr. 2013 - 31 Mar. 2017
    Chikenji Takako, SAITO Yuki, OZASA Yasuhiro, FUJIMIYA Mineko, IBA Kosuke
    An increased risk of carpal tunnel syndrome (CTS) has been reported in postmenopausal women. Fibrosis of subsynovial connective tissue (SSCT) is a prominent feature of CTS. Mesenchymal stem cells (MSCs) is considered to maintain the turnover of skeletal tissues in homeostasis. The purpose of this study was to assess the effect of the estradiol (E2) on SSCT-derived MSC (SSCT-MSC) of CTS patients in vitro. The proliferation activity of the SSCT-MSC was increased with E2. P16 mRNA expression and TP53 expression was significantly downregulated with E2. TGF-β was also downregulated with E2. We demonstrated that the effect of estradiol on SSCT-MSC in CTS patients, which increased the cell proliferation and inhibited the cellular senescence with downregulation of the TGF-β. Our findings suggested that the functional deterioration of SSCT-MSC might reside in the postmenopausal CTS patients, and relate to the homeostatic imbalance in SSCT fibrosis.
    Japan Society for the Promotion of Science, Grant-in-Aid for Young Scientists (B), Sapporo Medical University, Principal investigator, Competitive research funding, 25860144
  • 細胞老化から解明するうつ病の脳内慢性炎症メカニズムと新規治療法の開発　　　　　　　　　　　　　　　
    公益財団法人 秋山記念生命科学振興財団 2022 年度 研究助成(一般)
    公益財団法人 秋山記念生命科学振興財団, 北海道大学

Industrial Property Rights

  • 生体移植用細胞シート及びその製造方法　　　　　　　　　　　　　　　
    Patent right, 千見寺貴子
    特願2018-084565, 25 Apr. 2018
    特開WO2019/208688 A1
  • 間葉系幹細胞の賦活化剤への適応性を判定する方法　　　　　　　　　　　　　　　
    Patent right, 千見寺貴子
    特願2017-92030, 03 May 2017
    特開WO2018/199194 A1
  • 間葉系幹細胞の賦活化剤、賦活化された間葉系幹細胞およびその製造方法　　　　　　　　　　　　　　　
    Patent right, 千見寺貴子
    特願2017-86514, 25 Apr. 2017
    特許第6555691号

Media Coverage

  • 細胞老化の誘導機構を解明 慢性筋炎 骨格筋再生へ　　　　　　　　　　　　　　　
    Mar. 2020
    Other than myself
    北海道医療新聞
    [Paper]
  • Combination of exercise and cell-aging drug could help people with chronic inflammatory myopathy　　　　　　　　　　　　　　　
    Mar. 2020
    Other than myself
    The Medical News
    [Internet]
  • Cells must age for muscles to regenerate in muscle-degenerating diseases　　　　　　　　　　　　　　　
    Mar. 2020
    Other than myself
    MedicalXpress
    [Internet]
  • 北海道大学、エクササイズが骨格筋にもたらす“再生“と”変性“～間葉系前駆細胞の“老化“は骨格筋の再生を促す! 細胞老化を味方にする新しい治療戦略への期待～　　　　　　　　　　　　　　　
    Mar. 2020
    日経バイオテク
    [Internet]
  • 運動による「細胞の老化」が骨格筋の再生を促すことを発見　　　　　　　　　　　　　　　
    Mar. 2020
    Other than myself
    大学ジャーナル ON LINE
    [Internet]
  • SLEの抑うつ症状に老化細胞が関与、フィセチン経口投与で症状改善の可能性－　　　　　　　　　　　　　　　
    http://www.qlifepro.com/news/20211201/sle-3.html, [Internet]
  • 全身性エリテマトーデスの抑うつ症状に細胞老化が関与 ～老化細胞を標的とした新しい治療戦略への期待～　　　　　　　　　　　　　　　
    Other than myself
    日経バイオテク
    [Internet]

Others

  • 2022
    死体解剖資格 (系統解剖)