研究者データベース

研究者情報

マスター

アカウント(マスター)

  • 氏名

    青島 圭佑(アオシマ ケイスケ), アオシマ ケイスケ

所属(マスター)

  • 獣医学研究院 獣医学部門 臨床獣医科学分野

所属(マスター)

  • 獣医学研究院 獣医学部門 臨床獣医科学分野

独自項目

syllabus

  • 2020, 獣医病理学特論, Advanced Lecture on Veterinary Pathology, 博士後期課程, 獣医学院
  • 2020, 臨床疾病学特論, Advanced Lecture on Veterinary Clinical Diseases, 博士後期課程, 獣医学院
  • 2020, 総合専門臨床特論, Advanced and Comprehensive Studies on Integrated Specialized Veterinary Clinical Medicine, 博士後期課程, 獣医学院
  • 2020, アカデミックイングリッシュ, Academic English, 博士後期課程, 獣医学研究科
  • 2020, アカデミックイングリッシュ, Academic English, 博士後期課程, 獣医学院
  • 2020, アカデミックイングリッシュ, Academic English, 博士後期課程, 国際感染症学院

timetable

  • 博士後期課程, 国際感染症学院, 2020, アカデミックイングリッシュ
  • 博士後期課程, 獣医学研究科, 2020, アカデミックイングリッシュ
  • 博士後期課程, 獣医学研究科, 2020, 先端獣医科学特論A 国際獣医科学特論:臨床獣医学
  • 博士後期課程, 獣医学院, 2020, アカデミックイングリッシュ
  • 学士課程, 獣医学部, 2020, 病理学総論実習
  • 学士課程, 獣医学部, 2020, 病理学各論実習
  • 学士課程, 獣医学部, 2020, アドバンスト演習

researchmap

プロフィール情報

学位

  • 獣医師(2011年04月 北海道大学)
  • 博士 (獣医学)(2016年03月 北海道大学)
  • 日本獣医病理専門家協会会員(2016年04月)

プロフィール情報

  • 青島
  • 圭佑
  • ID各種

    201401007117561944

業績リスト

研究分野

  • ライフサイエンス / 分子生物学 / エピジェネティクス
  • ライフサイエンス / 腫瘍生物学 / 血管肉腫
  • ライフサイエンス / 獣医学 / 獣医病理学

経歴

  • 2017年04月 - 現在 北海道大学 大学院獣医学研究院 助教
  • 2018年04月 - 2020年05月 Yale School of Medicine Department of Pathology Visiting Research Scientist
  • 2015年11月 - 2017年03月 北海道大学 大学院獣医学研究科 助教
  • 2014年06月 - 2015年10月 北海道大学 大学院獣医学研究科 特任助教
  • 2013年04月 - 2014年06月 北海道大学 大学院獣医学研究科 日本学術振興会特別研究員 DC2

学歴

  • 2011年04月 - 2014年06月   北海道大学   大学院獣医学研究科
  • 2012年02月 - 2014年02月   東京大学   大学院農学生命科学研究科   特別研究学生
  • 2011年06月 - 2012年01月   京都大学   大学院医学研究科   特別研究学生
  • 2005年04月 - 2011年03月   北海道大学   獣医学部

受賞

  • 2014年09月 The 2nd Sapporo Summer Seminar for One Health, Special Award
     
    受賞者: 青島圭佑
  • 2011年03月 日本獣医師会長賞
     
    受賞者: 青島圭佑
  • 2006年06月 北海道大学 新渡戸賞
     
    受賞者: 青島圭佑

論文

  • Yoshiki Ichikawa, Mizuki Heishima, Kristin Vyhnal, Keisuke Aoshima, Kazuyoshi Sasaoka, Ryohei Kinoshita, Atsushi Kobayashi, Mitsuyoshi Takiguchi, Takashi Kimura
    Journal of Veterinary Diagnostic Investigation 2021年09月04日 [査読有り]
  • Kevin Christian M. Gulay, Keisuke Aoshima, Naoya Maekawa, Satoru Konnai, Atsushi Kobayashi, Takashi Kimura
    bioRxiv 2021年08月01日 [査読無し]
     
    AbstractHemangiosarcoma (HSA) is a malignant tumor derived from endothelial cells. Tumor-associated macrophages are one of the major components of tumor microenvironment and crucial for cancer development. The presence and function of macrophages in HSA have not been studied because there is no syngeneic model for HSA. In this study, we evaluated two mouse HSA cell lines and one immortalized mouse endothelial cells for their usefulness as syngeneic models for canine HSA. Our results show that the ISOS-1 cell line develops tumors with similar morphology to canine HSA. ISOS-1 cells highly express KDM2B and have similar KDM2B target expression patterns with canine HSA. Moreover, we determine that in both ISOS-1 and canine HSA tumors, macrophages are present as a major constituent of the tumor microenvironment. These macrophages are positive for CD204, an M2 macrophage marker, and express PD-L1. ISOS-1-conditioned medium can induce M2 polarization and PD-L1 expression in RAW264.7 mouse macrophage cell line. These results show that ISOS-1 can be used as a syngenic model for canine HSA and suggest that macrophages play an important role in immune evasion in HSA. Using the syngeneic mouse model for canine HSA, we can further study the role of immune cells in the pathology of HSA.
  • Kevin Christian Montecillo Gulay, Noriyuki Nagata, Keisuke Aoshima, Nozomi Shiohara, Atsushi Kobayashi, Mitsuyoshi Takiguchi, Takashi Kimura
    Journal of Comparative Pathology 187 63 - 67 2021年08月 [査読有り]
  • Sittinee Kulprasertsri, Shintaro Kobayashi, Keisuke Aoshima, Atsushi Kobayashi, Takashi Kimura
    Microbiology and immunology 2021年07月14日 [査読有り]
     
    Duck Tembusu virus (DTMUV) and Japanese encephalitis virus (JEV) are mosquito-borne flaviviruses. These two viruses infect ducks; however, they show different neurological outcomes. The mechanism of DTMUV- and JEV-induced neuronal death has not been well investigated. In the present study, we examined the differences in the mechanisms involved in virus-induced cell death and innate immune responses between DTMUV KPS54A61 strain and JEV JaGAr-01 strain using primary duck neurons (DN) and duck fibroblasts (CCL-141). DN and CCL-141 were permissive for the infection and replication of these two viruses, which upregulated the expression of innate immunity genes. Both DTMUV and JEV induced cell death via a caspase-3-dependent manner; however, DTMUV triggered more cell death than JEV did in both CCL-141 and DN. These findings suggest that DTMUV infection causes apoptosis in duck neurons and fibroblasts more strongly than JEV. Levels of the mRNA expression of innate immunity-related genes after DTMUV infection were generally higher than levels after JEV infection, suggesting that DTMUV-induced immune response in duck cells may exhibit toxic effect rather than protective effects. This article is protected by copyright. All rights reserved.
  • Atsushi Kobayashi, Yoshiko Munesue, Taishi Shimazaki, Keisuke Aoshima, Takashi Kimura, Shirou Mohri, Tetsuyuki Kitamoto
    Laboratory investigation; a journal of technical methods and pathology 2021年07月12日 [査読有り]
     
    Five sporadic Creutzfeldt-Jakob disease (CJD) strains have been identified to date, based on differences in clinicopathological features of the patients, the biochemical properties of abnormal prion proteins, and transmission properties. Recent advances in our knowledge about iatrogenic transmission of sporadic CJD have raised the possibility that the infectivity of sporadic CJD strains through peripheral routes is different from that of intracranial infection. To test this possibility, here we assessed systematically the infectivity of sporadic CJD strains through the peripheral route for the first time using a mouse model expressing human prion protein. Although the infectivity of the V2 and M1 sporadic CJD strains is almost the same in intracerebral transmission studies, the V2 strain infected more efficiently than the M1 strain through the peripheral route. The other sporadic CJD strains examined lacked infectivity. Of note, both the V2 and M1 strains showed preference for mice with the valine homozygosity at the PRNP polymorphic codon. These results indicate that the V2 strain is the most infectious sporadic CJD strain for infection through peripheral routes. In addition, these findings raise the possibility that individuals with the valine homozygosity at the PRNP polymorphic codon might have higher risks of infection through peripheral routes compared with the methionine homozygotes. Thus, preventive measures against the transmission of the V2 sporadic CJD strain will be important for the eradication of iatrogenic CJD transmission through peripheral routes.
  • Kevin Christian Montecillo Gulay, Keisuke Aoshima, Yuki Shibata, Hironobu Yasui, Qin Yan, Atsushi Kobayashi, Takashi Kimura
    Journal of genetics and genomics 2021年03月10日 [査読有り][通常論文]
     
    Epigenetic regulators have been implicated in tumorigenesis of many types of cancer; however, their roles in endothelial cell cancers such as canine hemangiosarcoma (HSA) have not been studied. In this study, we find that lysine-specific demethylase 2b (KDM2B) is highly expressed in HSA cell lines compared with normal canine endothelial cells. Silencing of KDM2B in HSA cells results in increased cell death in vitro compared with the scramble control by inducing apoptosis through the inactivation of the DNA repair pathways and accumulation of DNA damage. Similarly, doxycycline-induced KDM2B silencing in tumor xenografts results in decreased tumor sizes compared with the control. Furthermore, KDM2B is also highly expressed in clinical cases of HSA. We hypothesize that pharmacological KDM2B inhibition can also induce HSA cell death and can be used as an alternative treatment for HSA. We treat HSA cells with GSK-J4, a histone demethylase inhibitor, and find that GSK-J4 treatment also induces apoptosis and cell death. In addition, GSK-J4 treatment decreases tumor size. Therefore, we demonstrate that KDM2B acts as an oncogene in HSA by enhancing the DNA damage response. Moreover, we show that histone demethylase inhibitor GSK-J4 can be used as a therapeutic alternative to doxorubicin for HSA treatment.
  • T Ishizaki, J Yamazaki, J Jelinek, K Aoshima, T Kimura
    Research in veterinary science 132 521 - 526 2020年10月 [査読有り]
     
    Canine malignant melanoma is a common cancer with a high mortality rate. Although previous studies have evaluated various aspects of this tumour, the exact mechanism of tumourigenesis remains unknown. Epigenetic mechanisms, such as DNA methylation, have recently gained attention as aetiological factors for neoplasia in humans. This study aimed to analyse genome-wide DNA methylation patterns in canine malignant melanoma based on next-generation sequencing data. A total of 76,213 CpG sites, including 29,482 sites in CpG islands (CGIs), were analysed using next-generation sequencing of methylation-specific signatures, obtained by sequential digestion with enzymes, to compare normal oral mucosal samples from four healthy dogs, four canine melanoma cell lines (3 oral cavity and 1 skin), and five clinical samples of oral canine melanoma. Malignant melanoma showed increased methylation at thousands of normally unmethylated CpG sites in CGIs and decreased methylation at normally methylated CpG sites in non-CGIs. Interestingly, the promoter regions of 81-393 genes were hypermethylated; 23 of these genes were present in all melanoma cell lines and melanoma clinical samples. Among these 23 genes, six genes with "sequence-specific DNA binding" annotation were significantly enriched, including three Homeobox genes-HMX2, TLX2, and HOXA9-that may be involved in the tumourigenesis of canine malignant melanoma. This study revealed widespread alterations in DNA methylation and a large number of hypermethylated genes in canine malignant melanoma.
  • Meiling Zhang, Zongzhi Z. Liu, Keisuke Aoshima, Yangyi Zhang, Yongyan An, Asako Aoshima, Lok Hei Chan, Sabine M. Lang, Hongyi Sun, Zhenwei Tang, Sara J. Rutter, Carmen J. Booth, Veerle Bossuyt, Xiang Chen, Jon S. Morrow, Lajos Pusztai, David. L. Rimm, Mingzhu Yin, Qin Yan
    bioRxiv Cold Spring Harbor Laboratory 2020年09月10日 [査読無し][通常論文]
  • Ochbayar Erdemsurakh, Khurtsbaatar Ochirbat, Ulziisaikhan Gombosuren, Batbold Tserendorj, Baatarjargal Purevdorj, Batbaatar Vanaabaatar, Keisuke Aoshima, Atsushi Kobayashi, Takashi Kimura
    The Journal of veterinary medical science 2020年07月07日 [査読有り][通常論文]
     
    Glanders is a contagious and fatal equine disease caused by the gram-negative bacterium Burkholderia mallei.B. mallei is prevalent among horse populations in Asia, the Middle East, and South America. More than four million horses have been registered in Mongolia in 2020. However, the resent prevalence of glanders has not been well investigated. In this study, we aimed to investigate the seropositivity of B. mallei in horse populations in Mongolia using the complement fixation test (CFT) and Rose Bengal plate agglutination test (RBT). We randomly collected blood samples from horses in central and eastern Mongolia between 2018 and 2019. Of 337 horses, 26 (7.7%) and 28 (8.3%) were seropositive using RBT and CFT, respectively. Interestingly, seropositivity in horses resulting from crossbreeding of Mongolian native horses with thoroughbred horses was higher than that in Mongolian native horses. Our observations suggest that equine glanders are still endemic to Mongolia.
  • Teita Ishizaki, Jumpei Yamazaki, Shinji Meagawa, Nozomu Yokoyama, Keisuke Aoshima, Mitsuyoshi Takiguchi, Takashi Kimura
    Veterinary and comparative oncology 2020年03月18日 [査読有り][通常論文]
  • Minato E, Kobayashi A, Aoshima K, Fukushi H, Kimura T
    Microbiol Immunol 64 2 123 - 132 2020年02月 [査読有り][通常論文]
  • Gale M, Li Y, Cao J, Liu ZZ, Holmbeck MA, Zhang M, Lang SM, Wu L, Do Carmo M, Gupta S, Aoshima K, DiGiovanna MP, Stern DF, Rimm DL, Shadel GS, Chen X, Yan Q
    Cancer research 2019年11月 [査読有り][通常論文]
  • Morita A, Aoshima K*, Gulay KCM, Onishi S, Shibata Y, Yasui H, Kobayashi A, Kimura T, *Corresponding author
    Research in veterinary science 127 1 - 10 2019年10月 [査読有り][通常論文]
  • Minato E, Aoshima K, Kobayashi A, Ohnishi N, Sasaki N, Kimura T
    Veterinary pathology 56 5 300985819834616 - 710 2019年03月 [査読有り][通常論文]
  • Kobayashi A, Iwasaki Y, Takao M, Saito Y, Iwaki T, Qi Z, Torimoto R, Shimazaki T, Munesue Y, Isoda N, Sawa H, Aoshima K, Kimura T, Kondo H, Mohri S, Kitamoto T
    The American journal of pathology 189 6 1276 - 1283 2019年03月 [査読有り][通常論文]
  • Keisuke Aoshima*, Yuki Fukui, Kevin Christian Montecillo Gulay, Ochbayar Erdemsurakh, Atsuya Morita, Atsushi Kobayashi, Takashi Kimura, *Corresponding author
    BMC Veterinary Research 14 1 301  Springer Nature America, Inc 2018年12月 [査読有り][通常論文]
  • Kobayashi A, Qi Z, Shimazaki T, Munesue Y, Miyamoto T, Isoda N, Sawa H, Aoshima K, Kimura T, Mohri S, Kitamoto T, Yamashita T, Miyoshi I
    The American journal of pathology 189 3 677 - 686 2018年12月 [査読有り][通常論文]
  • H.M. Suranji Wijekoon, Sangho Kim, Eugene C. Bwalya, Jing Fang, Keisuke Aoshima, Kenji Hosoya, Masahiro Okumura
    Research in Veterinary Science 122 179 - 185 Elsevier {BV} 2018年12月 [査読有り][通常論文]
  • Raghda M. F. Abbas, Hassan T. Tag-El-Din-Hassan, Tussapon Boonyarattanasoonthorn, Keisuke Aoshima, Masami Morimatsu, Takashi Agui
    Japanese Journal of Veterinary Research 66 2 93 - 103 2018年05月01日 [査読有り][通常論文]
  • Yoshiko Munesue, Taishi Shimazaki, Zechen Qi, Norikazu Isoda, Hirofumi Sawa, Keisuke Aoshima, Takashi Kimura, Shirou Mohri, Tetsuyuki Kitamoto, Atsushi Kobayashi
    Neuroscience Letters 668 43 - 47 2018年03月06日 [査読有り][通常論文]
  • Aprilia Maharani, Keisuke Aoshima*, Shinichi Onishi, Kevin Christian Montecillo Gulay, Atsushi Kobayashi, Takashi Kimura. *Corresponding author
    Journal of Veterinary Medical Science 80 2 213 - 218 2018年02月01日 [査読有り][通常論文]
  • Yusuke Izumi, Keisuke Aoshima, Yuki Hoshino, Satoshi Takagi
    RESEARCH IN VETERINARY SCIENCE 112 222 - 228 2017年06月 [査読有り][通常論文]
  • Keisuke Aoshima, Takashi Kimura, Yuki Okada
    Methods in Molecular Biology 1605 259 - 270 2017年 [査読有り][通常論文]
  • Yuki Okada, Keisuke Aoshima
    CELL CYCLE 14 16 2541 - 2542 2015年08月 [査読有り][通常論文]
  • Keisuke Aoshima, Erina Inoue, Hirofumi Sawa, Yuki Okada
    EMBO REPORTS 16 7 803 - 812 2015年07月 [査読有り][通常論文]
  • Sawang Kesdangsakonwut, Yuji Sunden, Keisuke Aoshima, Yoshimi Iwaki, Masahiro Okumura, Hirofumi Sawa, Takashi Umemura
    NEUROPATHOLOGY 34 3 277 - 283 2014年06月 [査読有り][通常論文]
     
    Rabies is a fatal zoonotic disease for which no effective treatment measures are currently available. Rabies virus (RABV) has anti-apoptotic and anti-inflammatory properties that suppress nerve cell damage and inflammation in the CNS. These features imply that the elimination of RABV from the CNS by appropriate treatment could lead to complete recovery from rabies. Ten rabbits showing neuromuscular symptoms of rabies after subcutaneous (SC) immunization using commercially available vaccine containing inactivated whole RABV particles and subsequent fixed RABV (CVS strain) inoculation into hind limb muscles were allocated into three groups. Three rabbits received no further treatment (the SC group), three rabbits received three additional SC immunizations using the same vaccine, and four rabbits received three intrathecal (IT) immunizations, in which the vaccine was inoculated directly into the cerebrospinal fluid (the SC/IT group). An additional three naive rabbits were inoculated intramuscularly with RABV and not vaccinated. The rabbits exhibited neuromuscular symptoms of rabies within 4-8 days post-inoculation (dpi) of RABV. All of the rabbits died within 8-12 dpi with the exception of one rabbit in the SC group and all four rabbits in SC/IT group, which recovered and started to respond to external stimuli at 11-18 dpi and survived until the end of the experimental period. RABV was eliminated from the CNS of the surviving rabbits. We report here a possible, although still incomplete, therapy for rabies using IT immunization. Our protocol may rescue the life of rabid patients and prompt the future development of novel therapies against rabies.
  • Makino Y, Inoue E, Hada M, Aoshima K, Kitano S, Miyachi H, Okada Y
    Frontiers in cell and developmental biology 2 30  2014年 [査読有り][通常論文]
  • Keisuke Aoshima, Ai Baba, Yoshinori Makino, Yuki Okada
    PLOS ONE 8 10 e77715  2013年10月 [査読有り][通常論文]
  • Aoshima K, Okada Y
    Seikagaku. The Journal of Japanese Biochemical Society 85 4 278 - 283 4 2013年04月 [査読有り][通常論文]
  • Kensuke Nakamura, Masahiro Yamasaki, Tomohiro Osaki, Hiroshi Ohta, Noboru Sasaki, Keisuke Aoshima, Takashi Kimura, Mitsuyoshi Takiguchi
    JOURNAL OF THE AMERICAN ANIMAL HOSPITAL ASSOCIATION 48 5 327 - 330 2012年09月 [査読有り][通常論文]
  • Keisuke Aoshima, Yuji Sunden, Sachiyo Ishida, Kenji Ochiai, Takashi Umemura
    JOURNAL OF VETERINARY MEDICAL SCIENCE 73 10 1303 - 1308 2011年10月 [査読有り][通常論文]

MISC

  • ドキソルビシン耐性イヌ血管肉腫細胞株の樹立と薬剤耐性機構の解析
    森田 敦也, 青島 圭佑, 小林 篤史, 木村 享史 日本獣医学会学術集会講演要旨集 161 303 -303 2018年08月 [査読無し][通常論文]
  • イヌ血管肉腫におけるCXCR7シグナル伝達機構の解析
    大西 慎一, 青島 圭佑, 小林 篤史, 木村 享史 日本獣医学会学術集会講演要旨集 160 321 -321 2017年08月 [査読無し][通常論文]
  • マウス受精卵前核期におけるクロマチンダイナミクスの解析
    青島 圭佑, 岡田 由紀 日本獣医学会学術集会講演要旨集 156回 370 -370 2013年08月 [査読無し][通常論文]
  • 青島 圭佑, 岡田 由紀 生化学 85 (4) 278 -283 2013年04月 [査読無し][通常論文]
  • Y. Sunden, K. Aoshima, S. Ishida, K. Ochiai, T. Umemura JOURNAL OF COMPARATIVE PATHOLOGY 146 (1) 60 -60 2012年01月 [査読無し][通常論文]

担当経験のある科目(授業)

  • 獣医病理学特論北海道大学
  • 国際獣医科学特論:臨床獣医学北海道大学
  • 病理組織学実習北海道大学
  • 病理学総論実習北海道大学

所属学協会

  • 日本獣医病理専門家協会   日本分子生物学会   日本獣医学会   

共同研究・競争的資金等の研究課題

  • 日本学術振興会:科学研究費補助金 若手研究
    研究期間 : 2020年04月 -2022年03月 
    代表者 : 青島圭佑
  • イヌ血管肉腫におけるマウス疾患モデルの作製
    公益財団法人 栗林育英学術財団:研究助成事業
    研究期間 : 2020年09月 -2021年03月
  • イヌ血管肉腫未分化細胞のエピジェネティックな分化制御機構の解明
    日本学術振興会:科学研究費補助金 若手研究
    研究期間 : 2018年04月 -2020年03月 
    代表者 : 青島圭佑
  • 異常血管内皮細胞を制御する~血管肉腫と腫瘍血管の比較病理
    ノーステック財団:「研究開発助成事業」若手研究人材・ネットワーク育成補助金
    研究期間 : 2016年08月 -2017年03月 
    代表者 : 青島圭佑
  • 新規治療標的探索を目的としたイヌ血管肉腫におけるNotchシグナルの役割の解明
    秋山財団:研究助成<奨励>
    研究期間 : 2016年07月 -2017年03月 
    代表者 : 青島圭佑
  • マウス受精卵前核期におけるクロマチンダイナミクスの解析
    日本学術振興会:特別研究員奨励費 DC2
    研究期間 : 2013年04月 -2015年03月 
    代表者 : 青島圭佑


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