Researcher basic information

• 博士（スポーツ健康科学）, 立命館大学大学院スポーツ健康科学研究科, Mar. 2018

• https://researchmap.jp/aikedo?lang=en

• https://jglobal.jst.go.jp/detail?JGLOBAL_ID=201801004693843905

• 201801004693843905

• 性ホルモン
• female athlete
• Excercise
• Bone metabolism
• Nutrition

• Life Science, Nutrition science and health science

• Bachelor's degree program, School of Dental Medicine
• Doctoral (PhD) degree program, Graduate school of Dental Medicine

Research activity information

• Sep. 2025, 一般社団法人日本骨代謝学会, IFMRS Herbert Fleisch Workshop 2025 Travel Award
  池戸葵
• Jul. 2024, 一般社団法人日本骨代謝学会, ASBMR 2024 Travel Award
  Estrogen signaling in muscle mesenchymal progenitor cells positively regulates bone metabolism through Igfbp5
  池戸葵
• Oct. 2022, 一般社団法人日本骨代謝学会, IFMRS Herbert Fleisch Workshop 2022 Travel Award
  Aromatase in adipose tissue exerts osteoprotective function in male mice
  池戸葵
• Feb. 2022, 第29回日本ステロイドホルモン学会学術集会, 優秀演題賞
  池戸葵
• Mar. 2021, 一般社団法人日本骨代謝学会, ECTS 2021 Travel Award
  Estrogen receptor α in mature osteoblasts regulate the late stage of fracture healing.
  池戸葵

• UNC45B Reduction With Aging: A Myofiber‐Intrinsic Promoting Factor for Sarcopenia
  Taiga Mishima; Taiga Nagamune; Saori Tada; Daiki Watanabe; Nao Tokuda; Takashi Yamada; Akiko Hashimoto‐Hachiya; Sayaka Higo‐Yamamoto; Kohei Kido; Noriyuki Nagaoka; Aoi Ikedo; Yuuki Imai; Ryo Fujita; Seiya Mizuno; Satoru Takahashi; Katsutaka Oishi; Satoru Ato; Riki Ogasawara
  Aging Cell, 25, 5, Wiley, 20 Apr. 2026
  Scientific journal, ABSTRACT
  
  Skeletal muscle mass and force decline with age, and the loss of muscle force precedes muscle atrophy. However, the underlying mechanisms remain unclear. Here, we investigated the role of the myosin co‐chaperone, uncoordinated mutant number‐45 myosin chaperone B (UNC45B), in regulating muscle mass and force. UNC45B expression decreased in mouse gastrocnemius muscle with age, particularly at 24 months old, and adeno‐associated virus vector‐mediated knockdown of Unc45b in 3‐month‐old mouse triceps surae muscle first reduced plantar flexor torque and then decreased gastrocnemius muscle mass. In addition, Unc45b knockdown in the triceps surae muscle resulted in lower bone mineral density. While maximum Ca ²⁺ ‐activated force in mechanically skinned fibers was not affected by Unc45b knockdown, Unc45b knockdown decreased the ratio of depolarization‐induced force to the maximum Ca ²⁺ ‐activated force. We established tamoxifen‐inducible skeletal muscle‐specific Unc45b knockout ( Unc45b imKO) mice to investigate whether the muscle atrophy and weakness due to the loss of Unc45b impacts metabolism and behavior. We found that Unc45b imKO reduced muscle mass and force at a whole‐body level, but did not influence systemic glucose tolerance, insulin sensitivity, or the respiratory exchange ratio. However, Unc45b imKO mice reduced the amount of deeper non‐rapid eye movement sleep, locomotor activity, and body temperature during the sleep phase. We conclude that UNC45B is essential for maintaining fast‐twitch muscle mass and muscle force. In addition, Unc45b deficiency‐mediated muscle loss is also associated with bone fragility, decreased body temperature, and impaired sleep quality.
• Lithium and the Brain-Bone Axis: A Bridge between Osteoporosis and Alzheimer's Disease.
  Ji-Won Lee; Tomoka Hasegawa; Aoi Ikedo; Kaito Mizuno; Norio Amizuka; Sek Won Kong
  Current osteoporosis reports, 24, 1, 7, 7, 10 Feb. 2026, [International Magazine]
  English, Scientific journal, PURPOSE OF REVIEW: We evaluate the converging evidence positioning lithium as a systemic modulator of bone and brain health through shared molecular pathways. This review examines the molecular basis, preclinical data, and clinical observations suggesting that lithium-long established as first-line therapy for bipolar disorder-may simultaneously protect against osteoporosis and neurodegeneration as two clinical conditions increasingly recognized to share biological substrates. RECENT FINDINGS: Lithium inhibits glycogen synthase kinase-3β (GSK-3β), stabilizes β-catenin, and activates Wnt signaling in neurons and osteoblasts, while also modulating calcium-inositol homeostasis and suppressing NF-κB-mediated inflammation. Large observational studies report lower dementia incidence and reduced fracture risk in long-term lithium users, together with increases in bone mineral density. Declining brain lithium concentrations in patients with Alzheimer's disease raise the hypothesis that lithium may act as an essential micronutrient rather than solely a pharmacological agent. Bidirectional brain-bone crosstalk involving osteocalcin signaling and sclerostin transport across the blood-brain barrier provides a mechanistic basis for these pleiotropic effects. Lithium offers a unique paradigm for understanding and potentially treating age-related decline in multiple organ systems at subclinical dosage and concentration. However, observational study limitations, optimal dose uncertainties, and toxicity related to long-term usage concerns necessitate rigorous randomized controlled trials before broader clinical recommendations can be made. Future research should focus on optimizing formulation and patient selection to realize lithium's dual protective potential for bone and brain while minimizing risk.
• CTHRC1 promotes bone metastasis in prostate cancer.
  Yuichiro Sawada; Tadahiko Kikugawa; Tomoya Onishi; Osuke Arai; Hiroyuki Iio; Noriyoshi Miura; Shuhei Yoshida; Aoi Ikedo; Yuta Yanagihara; Noritaka Saeki; Iori Sakakibara; Balázs Győrffy; Takeshi Kishida; Yoichiro Okubo; Yoshiyasu Nakamura; Shinya Sato; Yohei Miyagi; Takashi Saika; Yuuki Imai
  International journal of cancer, 157, 11, 2399, 2412, 01 Dec. 2025, [International Magazine]
  English, Scientific journal, Prostate cancer causes a high frequency of bone metastases. The purpose of this study was to identify molecules that regulate prostate cancer bone metastasis as potential therapeutic and/or prognostic targets in prostate cancer, using integrative genome-wide data. Based on the biological characterization of prostate cancer cell lines and integrated big data analysis of clinical samples, we identified CTHRC1 as a candidate gene that regulates prostate cancer bone metastasis. The knockdown of CTHRC1 suppressed cell migration and cell adhesion, but not cell proliferation, in vitro and in vivo. In a mouse tibia xenograft model, CTHRC1 knockdown markedly suppressed metastatic growth of prostate cancer cells in the bone microenvironment. CTHRC1 also promoted in vitro osteoclast differentiation. The analysis of 343 human prostate cancer biopsy samples showed that CTHRC1 expression was positively correlated with bone metastasis, indicating that CTHRC1 could be a useful predictive marker for bone metastasis. Our findings illustrate the clinical relevance of CTHRC1 and demonstrate that CTHRC1 plays an important role in prostate cancer bone metastasis. CTHRC1 may be useful for predicting prostate cancer bone metastasis and may lead to the development of new methods for the prevention and treatment of metastasis.
• Estrogen signaling in PDGFRα+ cells positively regulates cortical bone metabolism via IGFBP5 in female mice
  Aoi Ikedo; Reina Aoki; Hiroshi Sakai; Noritaka Saeki; Yuta Yanagihara; Jonathan Moody; Miki Kojima; Tsukasa Kouno; Yoshinari Ando; Kazunori Hino; Tomofumi Kinoshita; Piero Carninci; Jay W Shin; Chung-Chau Hon; Akiyoshi Uezumi; Yoshiaki Kamei; Yuuki Imai
  JBMR Plus, Oxford University Press (OUP), 07 Nov. 2025
  Scientific journal, Abstract
  
  The prevalence of both osteoporosis and sarcopenia increases with age, and 60% of elderly sarcopenia patients also develop osteoporosis. However, the co-occurrence of osteoporosis and sarcopenia remains unclear. We performed single-cell 5’RNA-seq on human skeletal muscle tissues and investigated the enrichment of heritability for musculoskeletal traits in cell type specific cis-regulatory regions. We found the fibroblast-specific cis-regulatory regions are highly enriched in the heritability of bone mineral density (BMD). Using GWAS, we identified estrogen receptor α (ESR1) as a common transcription factor that correlated with both BMD and lean mass. We hypothesized that deficiency of estrogen signaling in fibroblast may attenuate musculoskeletal homeostasis. Therefore, we generated mice lacking Esr1 in PDGFRα (a fibroblast marker) + cells (Esr1ΔPα). Although muscle mass and grip strength were not different between groups, distal femoral BMD and cortical thickness were significantly lower in Esr1ΔPα compared to control. Bone histomorphometry showed that cortical bone in Esr1ΔPα exhibited a high turnover bone phenotype. Bulk RNA-seq using PDGFRα+ cells revealed that Igfbp5 expression was significantly higher in Esr1ΔPα compared to control. Furthermore, serum IGFBP5 level was significantly higher in Esr1ΔPα. IGFBP5 treatment in vitro significantly suppressed osteoblast differentiation and facilitated osteoclast differentiation. These results suggest that estrogen signaling in PDGFRα+ cells suppresses Igfbp5 expression, then maintains bone mass, indicating that estrogen signaling in PDGFRα+ cells plays a significant role in bone metabolism.
• Aromatase in adipose tissue exerts an osteoprotective function in male mice via phosphate regulation
  Aoi Ikedo; Michiko Yamashita; Maiko Hoshino; Yosuke Okuno; Megumi Koike; Minori Uga; Kazuya Tanifuji; Hiroko Segawa; Seiji Fukumoto; Yuuki Imai
  Journal of Bone and Mineral Research, Oxford University Press (OUP), 18 Sep. 2025, [Peer-reviewed]
  Scientific journal, Abstract
  
  Aromatase contributes to maintenance of bone mass because male patients with loss-of-function mutations of CYP19A1 exhibit bone loss. Treatment with aromatase inhibitor also causes bone loss in men and post-menopausal women, suggesting that part of the anabolic effect of testosterone in men is dependent on estradiol (E2) biosynthesized by aromatase in non-gonadal tissues. It remains unclear how locally biosynthesized E2 contributes to maintenance of bone mass. We examined the function of aromatase in local tissues rather than gonads using cell-type specific aromatase knockout (KO) mice. Because osteoblast-specific aromatase KO mice exhibited no bone phenotype, we focused on adipose tissue, known as a reservoir of steroid hormones and analyzed the bone phenotypes of adipose tissue-specific aromatase KO (AroΔaP2) mice. Sixteen-week-old male AroΔaP2 mice exhibited significantly lower bone mineral density in tibia and femur, especially in trabecular bone, than controls. Bone histomorphometry showed that AroΔaP2 mice exhibited an insufficient calcification bone phenotype with increased osteoid volume and width, and decreased osteoclast area and numbers. Moreover, serum phosphate, renal phosphate reabsorption, and FGF23 were significantly lower in AroΔaP2, suggesting that the insufficient calcification phenotype in AroΔaP2 was not caused by excessive FGF23 activities. Finally, we analyzed NaPi2a and NaPi2c, phosphate transporters localized in the kidney and found that protein levels in renal brush border membrane vesicles were lower in AroΔaP2. These results indicate that estrogens locally biosynthesized by aromatase in adipocytes can play a significant role in bone mass maintenance via regulation of phosphate reabsorption in the kidney by NaPi2.
• BMP3b regulates bone mass by inhibiting BMP signaling.
  Nao Kodama; Takuma Matsubara; Anna Yoshimura; Kenichi Nagano; Jun Hino; Kunikazu Tsuji; Aoi Ikedo; Yuuki Imai; Tatsuki Yaginuma; Quan Yuan; Kazumasa Morikawa; Yusuke Ono; Tomohiko Shirakawa; William N Addison; Izumi Yoshioka; Shoichiro Kokabu
  Bone, 190, 117303, 117303, 24 Oct. 2024, [International Magazine]
  English, Scientific journal, Bone morphogenetic protein 3b (BMP3b), also known as growth differentiation factor 10 (GDF10), is a non-osteogenic BMP highly expressed in the skeleton. Although in vitro studies have shown that BMP3b suppresses osteoblast differentiation, the physiological role of BMP3b in regulating bone mass in vivo remains unknown. Here, we show that BMP3b deletion in mice leads to a high bone mass phenotype via an unexpected novel mechanism involving de-repression of canonical BMP/Smad signaling. BMP3b null mice were viable, and exhibited no significant difference in body size compared to wildtype control. Trabecular bone parameters assessed by histomorphometry and μCT, revealed a significant increase in bone volume and bone mineral density. Expression of osteoblast-differentiation genes were elevated in bone tissue of BMP3b null mice, whereas expression of osteoclast-related genes remained unchanged. Consistent with this, Bmp3b was highly expressed in osteoblasts relative to osteoclast cells. Ex-vivo culture of primary bone marrow mesenchymal stem cells (BMSCs) and primary bone marrow-derived osteoclasts revealed that inactivation of BMP3b enhances osteogenesis without affecting osteoclastogenesis. Mechanistically, we found that BMP3b suppressed BMP4-induced Smad1/5 phosphorylation and inhibited the activity of a BMP4-driven Id-1 luciferase reporter. Protein-protein interaction assays revealed that BMP3b competitively interfered with the association of BMP4 and BMP type I receptors. These findings suggest that BMP3b regulates bone mass by acting as a BMP receptor antagonist. Thus, maintenance of bone mass involves antagonism of canonical BMP/Smad signaling by a member of the BMP family.
• KIF22 regulates mitosis and proliferation of chondrocyte cells.
  Hiroka Kawaue; Takuma Matsubara; Kenichi Nagano; Aoi Ikedo; Thira Rojasawasthien; Anna Yoshimura; Chihiro Nakatomi; Yuuki Imai; Yoshimitsu Kakuta; William N Addison; Shoichiro Kokabu
  iScience, 27, 7, 110151, 110151, 19 Jul. 2024, [International Magazine]
  English, Scientific journal, Point mutations in KIF22 have been linked to spondyloepimetaphyseal dysplasia with joint laxity, type 2 (SEMDJL2). Skeletal features of SEMDJL2 include short stature and joint laxity. Mechanisms underlying these limb abnormalities are unknown. Here in this manuscript, we have investigated the function of KIF22 in chondrocytes. Quantitative PCR and immunostaining revealed that Kif22 was highly expressed in proliferating-zone growth-plate chondrocytes. Kif22 knockdown resulted in defective mitotic spindle formation and reduced cell proliferation. Forced expression of SEMDJL-associated mutant Kif22 constructs likewise induced abnormal mitotic spindle morphology and reduced proliferation. Mice expressing a KIF22 truncation mutant had shorter growth plates and shorter tibial bones compared to wild-type mice. These results suggest that KIF22 regulates mitotic spindle formation in proliferating chondrocytes thereby linking the stunted longitudinal bone growth observed in SEMDJL2 to failures of chondrocyte division.
• Dietary restriction plus exercise change gene expression of Cxcl12 abundant reticular cells in female mice
  Aoi Ikedo; Yuuki Imai
  Journal of Bone and Mineral Metabolism, Springer Science and Business Media LLC, 01 Apr. 2024
  Scientific journal
• Bub1 suppresses inflammatory arthritis-associated bone loss in mice through inhibition of TNFα-mediated osteoclastogenesis.
  Shuhei Yoshida; Aoi Ikedo; Yuta Yanagihara; Tomohisa Sakaue; Noritaka Saeki; Yuuki Imai
  Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research, 27 Jan. 2024, [International Magazine]
  English, Scientific journal, Rheumatoid arthritis (RA) is an inflammatory autoimmune disease characterized by synovitis, bone and cartilage destruction, and increased fracture risk with bone loss. Although disease-modifying anti-rheumatic drugs (DMARDs) have dramatically improved clinical outcomes, these therapies are not universally effective in all patients due to the heterogeneity of RA pathogenesis. Therefore, it is necessary to elucidate the molecular mechanisms underlying RA pathogenesis, including associated bone loss, in order to identify novel therapeutic targets. In this study, we found that Budding uninhibited by benzimidazoles 1 (BUB1) was highly expressed in RA patients' synovium and murine ankle tissue with arthritis. As CD45+CD11b+ myeloid cells are a Bub1 highly expressing population among synovial cells in mice, myeloid cell-specific Bub1 conditional knockout (Bub1ΔLysM) mice were generated. Bub1ΔLysM mice exhibited reduced femoral bone mineral density (BMD) when compared to control mice under K/BxN serum-transfer arthritis (STA), with no significant differences in joint inflammation or bone erosion based on a semi-quantitative erosion score and histological analysis. Bone histomorphometry revealed that femoral bone mass of Bub1ΔLysM under arthritis was reduced by increased osteoclastic bone resorption. RNA-seq and subsequent Gene Set Enrichment Analysis (GSEA) demonstrated a significantly enriched NF-κB pathway among up-regulated genes in RANKL-stimulated bone marrow-derived macrophages (BMMs) obtained from Bub1ΔLysM mice. Indeed, osteoclastogenesis using BMMs derived from Bub1ΔLysM was enhanced by RANKL and TNFα or RANKL and IL-1β treatment compared to controls. Finally, osteoclastogenesis was increased by Bub1 inhibitor BAY1816032 treatment in BMMs derived from wildtype mice. These data suggest that Bub1 expressed in macrophages plays a protective role against inflammatory arthritis-associated bone loss through inhibition of inflammation-mediated osteoclastogenesis.
• The androgen receptor in mesenchymal progenitors regulates skeletal muscle mass via Igf1 expression in male mice.
  Hiroshi Sakai; Hideaki Uno; Harumi Yamakawa; Kaori Tanaka; Aoi Ikedo; Akiyoshi Uezumi; Yasuyuki Ohkawa; Yuuki Imai
  Cold Spring Harbor Laboratory, 22 Nov. 2023
  Androgens exert their effects primarily by binding to the androgen receptor (AR), a ligand-dependent nuclear receptor. While androgens have anabolic effects on skeletal muscle, previous studies reported that AR functions in myofibers to regulate skeletal muscle quality, rather than skeletal muscle mass. Therefore, the anabolic effects of androgens are exerted via extra-myofiber cells or tissues. In this context, the cellular and molecular mechanisms of AR in mesenchymal progenitors, which play a crucial role in maintaining skeletal muscle homeostasis, remain largely unknown. In this study, we demonstrated expression of AR in mesenchymal progenitors and found that targeted AR ablation in mesenchymal progenitors reduced limb muscle mass in mature adult, but not young or aged, male mice, although fatty infiltration of muscle was not affected. The absence of AR in mesenchymal progenitors led to remarkable perineal muscle hypotrophy, regardless of age, due to abnormal regulation of transcripts associated with apoptosis and proteolysis. Additionally, we revealed that AR in mesenchymal progenitors regulates the expression of insulin-like growth factor 1, which can increase skeletal muscle mass in a paracrine manner. These findings indicate that the anabolic effects of androgens indirectly regulate skeletal muscle mass via, at least in part, AR signaling in mesenchymal progenitors.
• Effect of hormonal therapy on the otoconial changes caused by estrogen deficiency
  Takahiro Nakata; Masahiro Okada; Eriko Nishihara; Aoi Ikedo; Sawa Asoh; Taro Takagi; Naohito Tokunaga; Naohito Hato; Yuuki Imai
  Scientific Reports, 12, 1, Springer Science and Business Media LLC, 30 Dec. 2022, [Peer-reviewed]
  Scientific journal, Abstract
  
  Benign paroxysmal positional vertigo (BPPV) is associated with menopause and/or osteopenia. Morphological changes in the otoconial layer have been reported after ovariectomy (OVX). Moreover, hormone replacement therapy decreases BPPV risk. However, knowledge concerning the effect of hormonal therapy on the otoconial changes caused by estrogen deficiency is limited. We aimed to examine the effect of hormonal therapy on otoconial changes caused by estrogen deficiency. We hypothesized that hormonal therapy could reduce otoconial changes caused by OVX. Eight-week-old C57BL/6 mice were divided into four groups: sham operation with implantation of vehicle (sham + v), OVX with implantation of vehicle (OVX + v), OVX with implantation of estradiol (E2) (OVX + E2), and OVX with implantation of raloxifene (RAL) (OVX + RAL) groups. Otoconial layer volume was measured by micro-CT at 4 weeks after OVX or the sham operation. The otic bullae were removed; immunohistochemistry was performed for estrogen receptor alpha and 4-hydroxynonenal. Otoconial layer volume was significantly higher in the OVX + v than in the sham + v group. E2 and RAL significantly reduced these changes in the endometrial layer. The staining of estrogen receptor alpha and 4-hydroxynonenal were stronger in the OVX + v than in the sham + v group but equal in the sham + v, OVX + E2, and OVX + RAL groups. These results indicate that E2 and RAL are effective against morphological changes of the otoconial layer caused by estrogen deficiency via oxidative stress reduction.
• Histone H3K27 demethylase, Utx, regulates osteoblast-to-osteocyte differentiation.
  Yuhan Xia; Aoi Ikedo; Ji-Won Lee; Tadahiro Iimura; Kazuki Inoue; Yuuki Imai
  Biochemical and biophysical research communications, 590, 132, 138, 28 Dec. 2021, [International Magazine]
  English, Scientific journal, Osteocytes are master regulators of skeletal homeostasis. However, little is known about the molecular mechanism of their differentiation. Epigenetic regulations, especially H3K27me3 modification, play critical roles in cell differentiation. Here, we found that H3K27me3 in the loci of osteocyte-expressing genes decreased during osteocyte differentiation and that H3K27me3 demethylase, Utx, was bound to the loci of those genes. To investigate the physiological functions of Utx in vivo, we generated late osteoblast-to-osteocyte specific Utx knockout mice using Dmp1-cre mice (UtxΔOcy/ΔOcy). Micro CT analyses showed that UtxΔOcy/ΔOcy displayed osteopenic phenotypes with lower bone volume and trabecular number, and greater trabecular separation. Bone histomorphometric analysis showed that bone mineralization and formation were significantly lower in UtxΔOcy/ΔOcy. Furthermore, Dmp1 expression and the number of osteocytes were significantly decreased in UtxΔOcy/ΔOcy. These results suggest that Utx in Dmp1-expressing osteoblast/osteocyte positively regulates osteoblast-to-osteocyte differentiation through H3K27me3 modifications in osteocyte genes. Our results provide new insight into the molecular mechanism of osteocyte differentiation.
• Estrogen receptor α in mature osteoblasts regulates the late stage of bone regeneration.
  Aoi Ikedo; Yuuki Imai
  Biochemical and biophysical research communications, 559, 238, 244, 05 May 2021, [Peer-reviewed], [Lead author], [International Magazine]
  English, Scientific journal, Estrogen deficiency impairs fracture healing and homeostasis of bone tissue. OVX-induced estrogen deficiency in mice attenuates fracture healing and changes the expression ratio of estrogen receptor (ER) α and ERβ in callus during the process of fracture healing. Therefore, ERs may be involved in the regulation of fracture healing. However, the roles of ERs in fracture healing are largely unknown. The purpose of this study was to clarify the significance of ERs during fracture healing using osteoblast-specific ER knockout mice in a mono-cortical drill hole bone regeneration model. The mature osteoblast-specific ER knockout mice were generated using osteocalcin (OCN)-Cre mice, and ERα and ERβ flox mice (OCN-Cre; ERαf/f, ERαΔOb/ΔOb and OCN-Cre; ERβf/f, ERβΔOb/ΔOb). Drill hole surgery was conducted on the tibiae of 8-week-old female mice. The mice were sacrificed 10 or 14 days after surgery and the bones were analyzed by DXA, μCT and bone histomorphometry. DXA analysis revealed that intact femoral BMD was significantly decreased in ERαΔOb/ΔOb mice compared with ERαf/f mice, but there was no difference in bone mass between ERβΔOb/ΔOb and ERβf/f mice. Micro CT analyses showed that the callus volume at the restricted drill hole site in tibiae was significantly less in ERαΔOb/ΔOb compared to ERαf/f mice only at day 14 but not at day 10. In addition to femoral BMD, there was no significant difference in callus volume between ERβΔOb/ΔOb and ERβf/f mice. Bone histomorphometric analyses showed that Ob.S/BS and N.Ob/B.Pm were significantly less in ERαΔOb/ΔOb mice compared with ERαf/f mice only at day 10. In addition, Oc.S/BS and N.Oc/B.Pm were significantly less in ERαΔOb/ΔOb mice compared with ERαf/f mice only at day 14. These results suggest that ERα but not ERβ in osteocalcin-positive osteoblasts may contribute to the late stage of bone regeneration.
• DNA maintenance methylation enzyme Dnmt1 in satellite cells is essential for muscle regeneration
  Hiroyuki Iio; Tadahiko Kikugawa; Yuichiro Sawada; Hiroshi Sakai; Shuhei Yoshida; Yuta Yanagihara; Aoi Ikedo; Noritaka Saeki; So-ichiro Fukada; Takashi Saika; Yuuki Imai
  Biochemical and Biophysical Research Communications, 534, 79, 85, Elsevier BV, Jan. 2021, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Epigenetic transcriptional regulation is essential for the differentiation of various types of cells, including skeletal muscle cells. DNA methyltransferase 1 (Dnmt1) is responsible for maintenance of DNA methylation patterns via cell division. Here, we investigated the relationship between Dnmt1 and skeletal muscle regeneration. We found that Dnmt1 is upregulated in muscles during regeneration. To assess the role of Dnmt1 in satellite cells during regeneration, we performed conditional knockout (cKO) of Dnmt1 specifically in skeletal muscle satellite cells using Pax7CreERT2 mice and Dnmt1 flox mice. Muscle weight and the cross-sectional area after injury were significantly lower in Dnmt1 cKO mice than in control mice. RNA sequencing analysis revealed upregulation of genes involved in cell adhesion and apoptosis in satellite cells from cKO mice. Moreover, satellite cells cultured from cKO mice exhibited a reduced number of cells. These results suggest that Dnmt1 is an essential factor for muscle regeneration and is involved in positive regulation of satellite cell number.
• Recent Insights into Long Bone Development: Central Role of Hedgehog Signaling Pathway in Regulating Growth Plate.
  Ryuma Haraguchi; Riko Kitazawa; Yukihiro Kohara; Aoi Ikedo; Yuuki Imai; Sohei Kitazawa
  International journal of molecular sciences, 20, 23, 20 Nov. 2019, [Peer-reviewed], [International Magazine]
  English, Scientific journal, The longitudinal growth of long bone, regulated by an epiphyseal cartilaginous component known as the "growth plate", is generated by epiphyseal chondrocytes. The growth plate provides a continuous supply of chondrocytes for endochondral ossification, a sequential bone replacement of cartilaginous tissue, and any failure in this process causes a wide range of skeletal disorders. Therefore, the cellular and molecular characteristics of the growth plate are of interest to many researchers. Hedgehog (Hh), well known as a mitogen and morphogen during development, is one of the best known regulatory signals in the developmental regulation of the growth plate. Numerous animal studies have revealed that signaling through the Hh pathway plays multiple roles in regulating the proliferation, differentiation, and maintenance of growth plate chondrocytes throughout the skeletal growth period. Furthermore, over the past few years, a growing body of evidence has emerged demonstrating that a limited number of growth plate chondrocytes transdifferentiate directly into the full osteogenic and multiple mesenchymal lineages during postnatal bone development and reside in the bone marrow until late adulthood. Current studies with the genetic fate mapping approach have shown that the commitment of growth plate chondrocytes into the skeletal lineage occurs under the influence of epiphyseal chondrocyte-derived Hh signals during endochondral bone formation. Here, we discuss the valuable observations on the role of the Hh signaling pathway in the growth plate based on mouse genetic studies, with some emphasis on recent advances.
• GPRC5Aは前立腺癌の細胞増殖と骨転移を促進する(GPRC5A facilitates cell proliferation and bone metastasis of prostate cancer)
  沢田 雄一郎; 飯尾 浩之; 柳原 裕太; 佐伯 法学; 池戸 葵; 榊原 伊織; 岸田 健; 宮城 洋平; 菊川 忠彦; 雑賀 隆史; 今井 祐記
  西日本泌尿器科, 81, 増刊, 145, 145, 西日本泌尿器科学会, Oct. 2019, [Peer-reviewed]
  English
• GPRC5A facilitates cell proliferation through cell cycle regulation and correlates with bone metastasis in prostate cancer.
  Yuichiro Sawada; Tadahiko Kikugawa; Hiroyuki Iio; Iori Sakakibara; Shuhei Yoshida; Aoi Ikedo; Yuta Yanagihara; Noritaka Saeki; Balázs GyŐrffy; Takeshi Kishida; Yoichiro Okubo; Yoshiyasu Nakamura; Yohei Miyagi; Takashi Saika; Yuuki Imai
  International Journal of Cancer, 5, Jul. 2019, [Peer-reviewed]
• The effects of resistance training on bone mineral density and bone quality in type 2 diabetic rats.
  Aoi Ikedo; Kohei Kido; Satoru Ato; Koji Sato; Ji-Won Lee; Satoshi Fujita; Yuuki Imai
  Physiological reports, 7, 6, e14046, Mar. 2019, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Resistance training (RT) has been known to be effective in maintaining and improving bone strength, which is based on bone mineral density (BMD) and bone quality. However, it is not clear whether RT is effective in improving bone strength in patients with type-2 diabetes mellitus (T2DM), who have a high risk of fracture. Therefore, we tested the effects of a 6-week RT regimen using percutaneous electrical stimulation in T2DM model rats, male Otsuka Long-Evans Tokushima Fatty (OLETF), and its control, Long-Evans Tokushima Otsuka (LETO). After 6 weeks of RT, tibial BMD in RT legs was significantly higher than that in control (CON) legs in both groups. In diaphyseal cortical bone, bone area/tissue area, and cortical thickness was significantly increased in RT legs compared with CON legs in both groups. Cortical porosity was highly observed in OLETF compared with LETO, but RT improved cortical porosity in both groups. Interestingly, trabecular number, trabecular thickness and trabecular space as well as BMD and bone volume/tissue volume in proximal tibial metaphyseal trabecular bone were significantly improved in RT legs compared with CON legs in both groups. In contrast, connectivity density and structural model index were not affected by RT. These results indicate that the 6-week RT regimen effectively increased BMD and improved bone quality in T2DM model rats as well as control rats. Therefore, RT may have the potential to improve bone strength and reduce fracture risk, even in patients with T2DM.
• The Effect of Ongoing Vitamin D and Low-Fat Milk Intake on Bone Metabolism in Female High-School Endurance Runners.
  Aoi Ikedo; Takuma Arimitsu; Toshiyuki Kurihara; Kumiko Ebi; Satoshi Fujita
  Journal of clinical medicine research, 10, 1, 13, 21, Jan. 2018, [Peer-reviewed], [International Magazine]
  English, Scientific journal, Background: Vitamin D and calcium are essential nutrients for bone health. In addition, vitamin D suppresses inflammatory cytokines and increases bone resorption. Therefore, improvements in bone health by calcium and vitamin D supplementation have the potential to not only improve calcium metabolism but also suppress inflammation associated with exercise training. The purpose of this study was to determine whether ongoing vitamin D supplementation and low-fat milk intake by female high-school endurance runners would improve bone metabolism by suppressing inflammatory cytokines and the parathyroid hormone (PTH). Methods: Twenty female high-school runners were assigned to a vitamin D supplement and low-fat milk intake group (MKD) or a control group (CON). Participants in the MKD group consumed a vitamin D supplement (1,000 IU/day) and low-fat milk (Ca 315 mg/day) for 6 months. Bone mineral density measurements, blood samples, and questionnaires (regarding menses and diet) were carried out. The UMIN Clinical Trials Registry number is UMIN000027854. Results: The 25-hydroxyvitamin D (25(OH)D) concentration in MKD was sustained and PTH concentration was decreased regardless of the state of menses. The correlation coefficients of 25(OH)D or PTH concentrations and bone metabolism markers were analyzed by partial correlation coefficient via adjusting the model for frequency of menses. CTX and 25(OH)D concentration were significantly and inversely correlated at baseline (r = -0.61, P < 0.01), 3 months (r = -0.54, P = 0.02), and 6 months (r = -0.53, P = 0.02). CTX and PTH were significantly and positively correlated at 3 months (r = 0.63, P < 0.01) and 6 months (r = 0.52, P = 0.02). The bone alkaline phosphatase (BAP)/CTX ratio and 25(OH)D concentration were significantly and positively correlated at 3 months (r = 0.59, P = 0.01) and 6 months (r = 0.56, P = 0.01). The BAP/CTX ratio and PTH were significantly and inversely correlated at 3 months (r = -0.59, P = 0.01) and 6 months (r = -0.58, P < 0.01). Conclusions: This study suggested that vitamin D and low-fat milk supplementation improves bone metabolism by sustaining the 25(OH)D concentration and decreasing the PTH concentration in female high-school endurance runners regardless of the state of menses.
• Examination of factors related to bone mineral density in female high school long distance runners and sprinters.
  Ikedo Aoi; Ishibashi Aya; Matsumiya Saori; Kaizaki Aya; Yuhaku Atsushi; Fujita Satoshi; Ebi Kumiko
  J Jpn Soc Nutr Food Sci., 70, 1, 9, 15, Japan Society of Nutrition and Food Science, Jan. 2017, [Peer-reviewed]
  Japanese, Scientific journal, The present study was conducted to compare bone mineral density (BMD) among long distance runners with sprinters, and to examine factors related to BMD at different bone sites among female high school track and field athletes. Thirty-seven adolescent female long distance runners (LDRs) and sprinters (SPRs) (16.1±0.8 yr old, LDR ［＞800 m］ n＝16, SPR ［100‐400 m］ n＝21) participated. We measured BMD and fat-free mass (FFM) by DXA. In addition, we assessed nutrient intake, physical activity, prior history of stress fracture and menstrual state using a questionnaire. BMD and FFM were significantly higher in SPRs than in LDRs. Multiple regression analysis showed that FFM was a significant covariate of BMD at all sites except for the spine. Seafood intake was a significant covariate of BMD in the arms, pelvis and total bone less head (TBLH) . BMI was a significant covariate of BMD in the pelvis. Differences in BMD between LDRs and SPRs were strongly influenced by FFM, and seafood intake was shown to be a factor contributing significantly to BMD among female high school track and field athletes.
• Comparison of Site-Specific Bone Mineral Densities between Endurance Runners and Sprinters in Adolescent Women
  Aoi Ikedo; Aya Ishibashi; Saori Matsumiya; Aya Kaizaki; Kumiko Ebi; Satoshi Fujita
  NUTRIENTS, 8, 12, 781, Dec. 2016, [Peer-reviewed]
  English, Scientific journal
• Influence of four weeks of n-3 polyunsaturated fatty acid supplementation on fat metabolism during prolonged exercise
  Aya Ishibashi; Hiroto Sasaki; Saori Matsumiya; Aoi Ikedo; Aya Kaizaki; Takafumi Hamaoka; Kazushige Goto; Kumiko Ebi
  Japanese Journal of Physical Fitness and Sports Medicine, 65, 2, 225, 235, Japanese Society of Physical Fitness and Sports Medicine, 2016, [Peer-reviewed]
  Japanese, Scientific journal

• Cxcl12 abundant reticular cells (CAR細胞) におけるエストロゲン受容体αの欠損は骨髄脂肪化を伴う骨量減少を引き起こす
  池戸葵; 李智媛; 今井祐記
  第44回日本骨代謝学会学術集会, 04 Jul. 2026, Oral presentation
  02 Jul. 2026 - 04 Jul. 2026
• エストロゲンおよび栄養・運動による骨代謝制御
  池戸 葵
  第44回日本骨代謝学会学術集会, 02 Jul. 2026, Nominated symposium
  02 Jul. 2026 - 04 Jul. 2026, [Invited]
• Estrogen receptor α deletion in Cxcl12-abundant reticular cells (CAR cells) causes bone loss and bone marrow adiposity.
  Aoi Ikedo
  1st Asia Pacific Herbert Fleisch Workshop 2025, 12 Nov. 2025, English, Oral presentation
  12 Nov. 2025 - 14 Nov. 2025
• 食事制限下の自発運動は雌性マウスにおける骨髄間葉系幹細胞の遺伝子発現を変化させる
  池戸葵
  第79回日本体力医学会大会, Sep. 2025, Poster presentation
  17 Sep. 2025 - 19 Sep. 2025
• Cxcl12 abundant reticular cells (CAR細胞) におけるエストロゲン受容体αの欠損は骨量減少および骨髄脂肪化を引き起こす
  池戸葵; 今井祐記
  第43回日本骨代謝学会学術集会, 24 Jul. 2025, Oral presentation
  24 Jul. 2025 - 26 Jul. 2025
• エストロゲンによる多臓器を介した骨代謝制御
  池戸葵; 今井祐記
  第43回日本骨代謝学会学術集会, 26 Jul. 2025, Nominated symposium
  [Invited]
• PDGFRα陽性間葉系前駆細胞におけるエストロゲンシグナルを介した筋骨連関作用
  池戸葵; 今井祐記
  第47回日本分子生物学会年会, 29 Nov. 2024, Public symposium
  [Invited]
• 脂肪組織で合成されたエストロゲンによる腎臓を介した骨代謝制御機構.
  池戸葵; 山下美智子; 星野麻衣子; 奥野陽亮; 宇賀稔; 谷藤和也; 瀬川博子; 福本誠二; 今井祐記
  第66回歯科基礎医学会学術大会, 02 Nov. 2024, Public symposium
  [Invited]
• 食事制限下の自発運動は雌性マウスにおける骨髄間葉系幹細胞の遺伝子発現を変化させる
  池戸葵; 今井祐記
  第78回日本体力医学会大会, Sep. 2024, Poster presentation
  02 Sep. 2024 - 04 Sep. 2024
• Estrogen signaling in muscle mesenchymal progenitor cells positively regulate bone metabolism through Igfbp5.
  Ikedo A.; Aoki R.; Sakai H.; Saeki N.; Moody J.; Kojima M.; Kouno T.; Ando Y.; Carninci P.; Shin JW; Hon CC; Uezumi A.; Kamei Y.; Imai Y.
  The 22nd Protein Island Matsuyama International Symposium, Sep. 2024, Poster presentation
  Sep. 2024
• Estrogen signaling in muscle mesenchymal progenitor cells positively regulates bone metabolism through Igfbp5.
  Ikedo A.; Aoki R.; Sakai H.; Moody J.; Shin JW; Hon CC; Kamei Y.; Imai Y.
  The American Society for Bone and Mineral Research, Sep. 2024, Poster presentation
  Sep. 2024
• PDGFRα陽性間葉系前駆細胞におけるエストロゲンシグナルによる運動器制御メカニズムの解明
  池戸葵; 青木玲奈; 酒井大史; Jonathan Moody; Jay W Shin; Chung-Chau Hon; 亀井義明; 今井祐記
  第42回日本骨代謝学会学術集会, Jun. 2024, Oral presentation
  29 Jun. 2024 - 02 Jul. 2024
• PDGFR α陽性間葉系前駆細胞におけるエストロゲンシグナルによる運動器制御メカニズムの解明
  池戸葵
  第10回骨格筋生物学研究会, Mar. 2024, Poster presentation
  08 Mar. 2024 - 10 Mar. 2024
• Aromatase in adipose tissue exerts osteoprotective function in male mice.
  Ikedo A.; Yamashita M.; Maiko Hoshino; Minori Uga; Hiroko Segawa; Seiji Fukumoto; Yuuki Imai
  The 21st Protein Island Matsuyama International Symposium, Sep. 2023, Poster presentation
  Sep. 2023
• 脂肪組織中のAromataseによる雄性骨量制御機構の解明
  池戸葵; 山下美智子; 星野麻衣子; 宇賀稔; 瀬川博子; 福本誠二; 今井祐記
  第41回日本骨代謝学会学術集会, Jul. 2023, Oral presentation
  27 Jul. 2023 - 29 Jul. 2023
• Relative Energy Deficiency in Sport (RED-S)による骨髄間葉系幹細胞機能変容の解明
  池戸葵; 今井祐記
  第41回日本骨代謝学会学術集会, Jul. 2023, Poster presentation
  27 Jul. 2023 - 29 Jul. 2023
• Aromatase in adipose tissue exerts osteoprotective function in male mice.
  Ikedo A.; Yamashita M.; Hoshino M.; Fukumoto S.; Imai Y.
  4th Herbert Fleisch Workshop, Nov. 2022, Oral presentation
  20 Nov. 2022 - 22 Nov. 2022
• Relative Energy Deficiency in Sport (RED-S)による骨髄間葉系幹細胞機能変容の解明
  池戸葵; 今井祐記
  第 77 回日本体力医学会大会, Sep. 2022, Poster presentation
  21 Sep. 2022 - 23 Sep. 2022
• Relative Energy Deficiency in Sport (RED-S) による骨髄間葉系幹細胞機能変容の解明
  池戸葵
  第21回運動器科学研究会, Sep. 2022, Oral presentation
  16 Sep. 2022 - 17 Sep. 2022
• Aromataseによる雄性骨量制御機構の解明
  池戸葵; 山下美智子; 星野麻衣子; 福本誠二; 今井祐記
  第40回日本骨代謝学会学術集会, Jul. 2022, Oral presentation
  22 Jul. 2022 - 23 Jul. 2022
• 雄性骨量制御機構に対するAromataseの作用機序解明
  池戸葵; 山下美智子; 星野麻衣子; 福本誠二; 今井祐記
  第7回日本骨免疫学会, Jun. 2022, Poster presentation
  29 Jun. 2022 - 01 Jul. 2022
• 脂肪組織におけるAromataseは骨量維持に作用する
  池戸葵; 山下美智子; 星野麻衣子; 今井祐記
  第29回日本ステロイドホルモン学術集会, 19 Feb. 2022, Oral presentation
  19 Feb. 2022 - 19 Feb. 2022
• 成熟骨芽細胞のエストロゲン受容体αは骨再生過程の後期を制御する
  池戸葵; 今井祐記
  第39回日本骨代謝学会学術集会, Oct. 2021, Oral presentation
  08 Oct. 2021 - 10 Oct. 2021
• 脂肪組織におけるAromataseは骨量維持に作用する
  池戸葵; 山下美智子; 星野麻衣子; 今井祐記
  第76回日本体力医学会大会, Sep. 2021, Poster presentation
  17 Sep. 2021 - 19 Sep. 2021
• Estrogen receptor α in mature osteoblasts regulate the late stage of bone regeneration.
  Ikedo A.; Imai Y.
  The 19th Protein Island Matsuyama International Symposium, 08 Sep. 2021, Poster presentation
  08 Sep. 2021
• Estrogen receptor α in mature osteoblasts regulates the late stage of fracture healing.
  Ikedo A.; Imai Y.
  48th Annual European Calcified Tissue Society Congress, May 2021, Poster presentation
  May 2021
• 脂肪組織の Aromatase は骨量維持に作用する
  池戸葵; 山下美智子; 星野麻衣子; 今井祐記
  第38回日本骨代謝学会学術集会, Oct. 2020, Oral presentation
  09 Oct. 2020 - 12 Oct. 2020
• 脂肪組織におけるAromataseは骨量維持に作用する
  池戸葵; 山下美智子; 星野麻衣子; 今井祐記
  第27回日本ステロイドホルモン学術集会, 02 Nov. 2019, Oral presentation
  02 Nov. 2019 - 02 Nov. 2019
• 脂肪組織におけるAromataseは骨量維持に作用する
  池戸葵; 山下美智子; 星野麻衣子; 今井祐記
  第74回日本体力医学会大会, Sep. 2019, Poster presentation
  19 Sep. 2019 - 21 Sep. 2019
• Aromatase in adipose tissue exerts an osteoprotective function.
  Ikedo A.; Yamashita M.; Hoshino M.; Imai Y.
  The 17th Protein Island Matsuyama International Symposium, Sep. 2019, Poster presentation
  10 Sep. 2019 - 11 Sep. 2019
• 2型糖尿病モデルラットに対するレジスタンストレーニングの効果
  池戸葵; 木戸康平; 阿藤聡; 佐藤幸治; 今井祐記; 藤田聡
  第19回運動器科学研究会, Sep. 2018, Oral presentation
  07 Sep. 2018 - 07 Sep. 2018
• 高校生女子長距離選手におけるビタミンDサプリメント及び低脂肪乳飲料の併用摂取が骨代謝及び骨量に与える影響の検討
  池戸葵; 有光琢磨; 栗原俊之; 海老久美子; 藤田聡
  第4回Neo Vitamin D Workshop学術集会, Aug. 2018, Oral presentation
  24 Aug. 2018 - 25 Aug. 2018
• 運動前のビタミンDと低脂肪乳摂取が運動誘発性の骨吸収に及ぼす影響の検討
  池戸葵; 藤田聡
  第72回日本体力医学会大会, Sep. 2017, Oral presentation
  16 Sep. 2017 - 18 Sep. 2017
• 2型糖尿病モデルラットに対する長期的なレジスタンス運動が骨組織に与える効果
  池戸葵; 木戸康平; 阿藤聡; 佐藤幸治; 今井祐記; 藤田聡
  第35回日本骨代謝学会学術集会, Jul. 2017, Oral presentation
  27 Jul. 2017 - 29 Jul. 2017
• The effect of Perilla frutescens extract ingestion on downhill running-induced muscle damage and inflammatory response.
  Ikedo A.; Goto M.; Shinohara Y.; Isaka T.; Fujita S.
  The 25th Annual Meeting of International Congress on Nutrition and Integrative Medicine, 08 Jul. 2017, Poster presentation
  08 Jul. 2017 - 09 Jul. 2017
• Influence of 25(OH)D, parathyroid hormone and cytokines on bone resorption during acute vigorous running.
  Ikedo A.; Imai M.; Fujita S.
  American College of Sports Medicine’ s 64nd Annual Meeting, May 2017
  30 May 2017 - 03 Jun. 2017
• 2型糖尿病モデルラットの骨に対するレジスタンストレーニングの効果
  池戸葵; 木戸康平; 阿藤聡; 佐藤幸治; 今井祐記; 藤田聡
  第5回骨格筋生物学研究会, Mar. 2017, Oral presentation
  03 Mar. 2017 - 05 Mar. 2017
• 長時間走運動により誘発されるPTHとサイトカインが骨吸収に及ぼす影響
  池戸葵; 藤田聡
  第71回日本体力医学会大会, Sep. 2016, Oral presentation
  23 Sep. 2016 - 25 Sep. 2016
• Site-specific differences in the bone mineral density of adolescent sprinters and long distance runners.
  Ikedo A.; Ishibashi A.; Matsumiya S.; Kaizaki A.; Ebi K.; Fujita S.
  American College of Sports Medicine’ s 63nd Annual Meeting, May 2016
  31 May 2016
• 成長期女子アスリートの食事と骨代謝マーカーの変化；4ヵ月間の追跡調査
  池戸葵; 石橋彩; 松宮さおり; 海崎彩; 佐藤幸治; 祐伯敦史; 藤田聡; 海老久美子
  日本スポーツ栄養学会 第2回大会, Jul. 2015, Oral presentation
  04 Jul. 2015 - 05 Jul. 2015
• Relationship between nutritional intake and bone resorption among female high school track and field athletes.
  Ikedo A.; Ishibashi A.; Saori M.; Kaizaki A.; Sato K.; Fujita S.; Ebi K.
  Asian Congress of Nutrition, May 2015, Poster presentation
  14 May 2015 - 18 May 2015
• Relationship between bone mineral density and nutritional intake among female high school track and field athletes
  Ikedo A.; Ishibashi A.; Saori M.; Kaizaki A.; Yuhaku A.; Fujita S.; Ebi K.
  The European Society for Clinical Nutrition and Metabolism, Oct. 2014, Poster presentation
  06 Oct. 2014 - 09 Oct. 2014
• 高校生女子陸上競技選手における疲労骨折リスクと骨密度に関する検討
  池戸葵; 松宮さおり; 石橋彩; 海崎彩; 佐藤幸治; 祐伯敦史; 浜岡隆文; 藤田聡; 海老久美子
  第1回日本スポーツ栄養学会, Jul. 2014, Oral presentation
  11 Jul. 2014 - 13 Jul. 2014
• 高校生女子陸上競技選手の身体組成と疲労骨折リスクの関連
  池戸葵; 藤田聡; 石橋彩; 松宮さおり; 海崎彩; 海老久美子
  第68回日本栄養・食糧学会, May 2014, Oral presentation
  30 May 2014 - 01 Jun. 2014

• 日本骨免疫学会
• 日本栄養食糧学会
• 日本体力医学会
• 日本骨代謝学会

• 脂肪組織中のAromataseによる骨量制御機構の解明
  2022年度 医学系研究助成
  Jul. 2022 - May 2027
  池戸葵
  公益財団法人 武田科学振興財団, Principal investigator
• エストロゲンによる骨髄間葉系間質細胞の分化制御機構の解明
  科学研究費助成事業
  01 Apr. 2024 - 31 Mar. 2027
  池戸 葵; 今井 祐記
  日本学術振興会, 基盤研究(C), 愛媛大学, 24K12418
• エネルギー制限下での運動に伴う骨脆弱化を予測する液性因子の探索
  2026年度研究助成 一般
  Jun. 2026 - Mar. 2027
  池戸 葵
  公益財団法人 秋山記念生命科学振興財団, Principal investigator
• Cxcl12 abundant reticular cells (CAR細胞) におけるエストロゲン受容体α (ERα) の欠損は骨髄脂肪化を伴う骨量減少を引き起こす
  海外学会等出席研究 交流助成
  Jun. 2026 - Mar. 2027
  池戸 葵
  公益財団法人 伊藤医薬学術交流財団, Principal investigator
• スポーツによる相対的エネルギー不足 (REDs) における骨髄間葉系幹細胞の機能解析
  第62回 学術研究奨励金
  Jul. 2024 - Jul. 2025
  公益財団法人 三島海雲記念財団, Principal investigator
• アロマターゼ阻害薬による乳癌治療関連骨量減少症のメカニズム解明
  科学研究費助成事業
  Apr. 2022 - Mar. 2025
  亀井 義明; 今井 祐記; 池戸 葵
  日本学術振興会, 基盤研究(C), 愛媛大学, 22K09358
• 若年女性アスリートのエストロゲン分泌異常による骨代謝障害の機序解明
  科学研究費助成事業 若手研究
  01 Apr. 2021 - 31 Mar. 2024
  池戸 葵
  エストロゲン欠乏による骨量低下は、閉経後女性のみならず思春期女性やアスリートにおいても問題視されており、骨折や疲労骨折の治癒遷延の大きな原因の一つとなっている。そこで、骨折修復部では、間葉系間質細胞が増殖し骨芽細胞へ分化していくことから、我々は、間葉系間質細胞であるCXCL12-abundant reticular cells (CAR細胞) に着目した。CAR細胞は、骨折修復への寄与率が高く、エストロゲン受容体α (ERα) 発現量が高いにも関わらず、エストロゲンによる制御機構は全く不明である。本研究では、骨髄特異的間葉系幹細胞に対するエストロゲンの役割を明らかにし、骨恒常性の維持や骨折治癒に対する制御機構を解明することを目的とした。
  現在、Ebf3-CreERT2マウスとエストロゲン受容体α(ERα) floxマウスの交配により、CAR細胞特異的ERα遺伝子欠損マウスの作出に成功している。また、このマウスの骨表現系を確認すると共に、完全骨折モデルを用いた骨折治癒過程の評価を実施している。フローサイトメトリー法を用いて、コントロールマウスとERα欠損マウスの無処置の骨髄から、CAR細胞を単離し、各細胞のRNAから遺伝子発現をqPCRで確認すると、いくつかの遺伝子発現量に変化が認められた。この結果を基に、細胞の自己複製能や増殖能、分化能について評価していく予定である。
  今後は、サンプル数を増やし、CAR細胞特異的ERα欠損マウスの表現型を確認していく。表現型を確認した後、RNA-seqによる遺伝子発現網羅解析を行い、標的遺伝子の同定を目指す。
  日本学術振興会, 若手研究, 愛媛大学, 21K16688
• エストロゲンによる間葉系幹細胞を介した骨折治癒制御機構の解明
  2021年度 Ⅲ研究助成 ②再生医療研究
  Dec. 2021 - Mar. 2023
  池戸葵
  公益財団法人 テルモ生命科学振興財団, Principal investigator
• スポーツによる相対的エネルギー不足（RED-S）による骨髄間葉系幹細胞機能変容の解明
  第３７回若手研究者のための健康科学研究助成
  Jul. 2021 - Jan. 2023
  池戸葵
  公益財団法人 明治安田厚生事業団, Principal investigator
• エストロゲン欠乏による骨折治癒遷延の分子メカニズム解明と治癒促進法の開発
  科学研究費助成事業 若手研究
  Apr. 2019 - Mar. 2021
  池戸 葵
  日本学術振興会, Principal investigator, Competitive research funding
• エストロゲン欠乏による疲労骨折治癒遷延からの競技復帰を促進する治療標的の探索
  スポーツチャレンジ研究助成 第13期生
  Apr. 2019 - Mar. 2020
  池戸 葵
  公益財団法人ヤマハ発動機スポーツ振興財団, Principal investigator, Competitive research funding
• 激しい運動はビタミンDの消費を促進するか？ーアスリートのビタミンDの必要性ー
  第40回公益財団法人石本記念デサントスポーツ科学振興財団学術研究
  Apr. 2018 - Oct. 2018
  池戸 葵
  公益財団法人石本記念デサントスポーツ科学振興財団, Principal investigator, Competitive research funding
• 女子アスリートの疲労骨折予防に向けたビタミンD補給法の検討
  スポーツチャレンジ研究助成 第10期生
  Apr. 2016 - Mar. 2017
  池戸 葵
  公益財団法人ヤマハ発動機スポーツ振興財団, Principal investigator, Competitive research funding
• 乳飲料およびビタミンDサプリメントの併用摂取におけるアスリートの疲労骨折予防効果の検討
  「牛乳乳製品健康科学」 学術研究
  Apr. 2016 - Jan. 2017
  藤田聡; 池戸 葵
  一般社団法人 Jミルク内「乳の学術連合」, Principal investigator, Competitive research funding