2025/08/12 更新

写真a

アオヌマ タツヤ
青沼 達也
AONUMA Tatsuya
所属
病院 診療科 内科(循環器・腎臓)
外部リンク

学位

  • 博士課程 ( 2016年6月   旭川医科大学 )

学歴

  • 旭川医科大学   医学研究科

    - 2016年6月

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    国名: 日本国

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経歴

  • 旭川医科大学   助教

    2021年4月 - 現在

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  • 旭川医科大学   客員教員(助教)

    2016年7月 - 2021年3月

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  • 旭川医科大学   大学院生(博士課程)

    2012年4月 - 2016年6月

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留学歴

  • 2019年4月 - 2021年2月   インディアナ大学医学部   ポスドク研究員

  • 2017年4月 - 2019年3月   オーガスタ大学   ポスドク研究員

論文

  • Periostin is a Pivotal Target of microRNA-150-5p in Cardiac Fibroblast Activation and Chronic Myocardial Infarction. 国際誌

    Taiki Hayasaka, Bruno Moukette, Marisa N Sepúlveda, Satoshi Kawaguchi, Tatsuya Aonuma, Hamedane Moustapha, Lei Yang, Meena S Madhur, Suthat Liangpunsakul, Il-Man Kim

    JACC. Basic to translational science   10 ( 8 )   101330 - 101330   2025年7月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Our prior studies have revealed that miR-150-5p (miR-150) attenuated cardiac dysfunction in mice, which overexpressed a long noncoding RNA called myocardial infarction-associated transcript during myocardial infarction or harbored cardiac-specific abrogation of β-arrestin-mediated β1-adrenergic receptor signaling during chronic catecholamine stimulation. Although previous studies have shown the importance of miR-150 in heart failure, details surrounding its actions remain elusive in part because of (1) the lack of detailed mechanistic insight by which this small noncoding RNA induces myocardial protection and (2) the absence of definitive studies using appropriate mouse models to establish its direct functional relationship with key downstream targets. In the current study, we provide strong evidence that fibrotic periostin is a significant downstream target of miR-150 repression in ischemic mouse hearts. To the best of our knowledge, this is the first study to directly establish the functional link between miR-150 and periostin in murine myocardial infarction and primary adult human cardiac fibroblast activation.

    DOI: 10.1016/j.jacbts.2025.101330

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  • Fatal Outcome Due to Pulmonary Arterial Intramural Hematoma Associated With Stanford Type A Acute Aortic Dissection: A Case Report. 国際誌

    Yudai Shiwaku, Tatsuya Aonuma, Kanako Matsuda, Takahiro Shiokoshi, Naoki Nakagawa

    Cureus   17 ( 6 )   e85969   2025年6月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    Stanford type A acute aortic dissection (AAD) is associated with a poor prognosis. Pulmonary artery intramural hematoma (PA-IMH) is an underrecognized complication of AAD. Here, we report a case of an 86-year-old man diagnosed with Stanford type A AAD. During emergency transfer to a tertiary care center with cardiovascular surgical capabilities, the patient experienced a cardiac arrest during transport by an ambulance and was subsequently pronounced dead. Postmortem computed tomography (CT) revealed right PA compression and wall thickening consistent with PA-IMH. Additionally, associated ground-glass opacity in the right lower lobe suggested alveolar hemorrhage, likely contributing to circulatory collapse, followed by cardiac arrest and death. We identified two important clinical issues. First, in cases of AAD, PA-IMH should be considered a potential complication when contrast-enhanced CT reveals obstruction or stenosis of the PA. Second, some cases of PA-IMH may present with alveolar hemorrhage, an important prognostic factor of PA-IMH that should be identified using CT with lung window settings.

    DOI: 10.7759/cureus.85969

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  • Cardiomyocyte-restricted MIAT deletion is sufficient to protect against murine myocardial infarction

    Taiki Hayasaka, Satoshi Kawaguchi, Marisa N. Sepúlveda, Jian-peng Teoh, Bruno Moukette, Tatsuya Aonuma, Meena S. Madhur, Ankit A. Desai, Suthat Liangpunsakul, Simon J. Conway, Il-man Kim

    Cell Death Discovery   11 ( 1 )   2025年2月

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    掲載種別:研究論文(学術雑誌)   出版者・発行元:Springer Science and Business Media LLC  

    Abstract

    Myocardial infarction-associated transcript (MIAT), an intergenic long noncoding RNA (lncRNA), is conserved between rodents and humans and is directly linked to maladaptive cardiac remodeling in both patients and mouse models with various forms of heart failure (HF). We previously reported attenuation of cardiac stress, apoptosis, and fibrosis in a murine model of myocardial infarction (MI) with global MIAT ablation. Our transcriptomic profiling and mechanistic studies further revealed MIAT-induced activation of maladaptive genes, such as Hoxa4, Fmo2, Lrrn4, Marveld3, and Fat4. However, the source of MIAT and its contribution to MI and HF remain unknown. In this study, we generate a novel cardiomyocyte (CM)-specific MIAT conditional knockout mouse model, which exhibits improved cardiac function after MI. We further report that CM-specific MIAT ablation is sufficient to reduce cardiac damage, apoptosis, and fibrosis following chronic MI. Mechanistically, CM-specific MIAT deletion in mice leads to decreased expression of proapoptotic and pathological profibrotic genes, such as p53, Bak1, Col3a1, Col6a1, Postn, and Snail1 after chronic MI. These results enable us to begin to dissect cell-specific contributions to MIAT signaling and bolster the idea that MIAT plays a direct pathological role in CMs after MI.

    DOI: 10.1038/s41420-025-02352-9

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    その他リンク: https://www.nature.com/articles/s41420-025-02352-9

  • A case of rapid rupture of a calcified amorphous tumor observed by echocardiography. 国際誌

    Kentaro Shirakura, Ryohei Ushioda, Masahiro Tsutsui, Shingo Kunioka, Nobuhiro Mochizuki, Tatsuya Aonuma, Naoko Kawabata, Erika Saitoh, Naoki Nakagawa, Hiroyuki Kamiya

    Journal of surgical case reports   2025 ( 2 )   rjaf064   2025年2月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    A calcified amorphous tumor (CAT) of the heart is a rare, non-neoplastic, intracavitary cardiac mass. Histological examination reveals the presence of calcified and amorphous fibrous material with underlying chronic inflammation. Some studies have reported that CAT typically exhibits rapid growth. However, we observed a case in which CAT unexpectedly ruptured within approximately two weeks. There was no cerebral infarction or significant valvular disease, therefore we were not sure about the indication for surgery; however considering the epidemiological possibility of CAT, we decided to operate and were able to treat the patient without complications.

    DOI: 10.1093/jscr/rjaf064

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  • MicroRNA-150 Deletion from Adult Myofibroblasts Augments Maladaptive Cardiac Remodeling Following Chronic Myocardial Infarction. 国際誌

    Satoshi Kawaguchi, Marisa N Sepúlveda, Jian-Peng Teoh, Taiki Hayasaka, Bruno Moukette, Tatsuya Aonuma, Hyun Cheol Roh, Meena S Madhur, Il-Man Kim

    Biomolecules   14 ( 12 )   2024年12月

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    記述言語:英語   掲載種別:研究論文(学術雑誌)  

    MicroRNA (miR: small noncoding RNA)-150 is evolutionarily conserved and is downregulated in patients with diverse forms of heart failure (HF) and in multiple mouse models of HF. Moreover, miR-150 is markedly correlated with the outcome of patients with HF. We previously reported that systemic or cardiomyocyte-derived miR-150 in mice elicited myocardial protection through the inhibition of cardiomyocyte death, without affecting neovascularization and T cell infiltration. Our mechanistic studies also showed that the protective roles of miR-150 in ischemic mouse hearts and human cardiac fibroblasts were, in part, attributed to the inhibition of fibroblast activation via the repression of multiple profibrotic genes. However, the extent to which miR-150 expression in adult myofibroblasts (MFs) modulates the response to myocardial infarction (MI) remains unknown. Here, we develop a novel 4-hydroxytamoxifen-inducible MF-specific miR-150 conditional knockout mouse model and demonstrate that the mouse line exhibits worse cardiac dysfunction after MI. Our studies further reveal that miR-150 ablation selectively in adult MFs exacerbates cardiac damage and apoptosis after chronic MI. Lastly, MF-specific miR-150 deletion in adult mice promotes the expression of proinflammatory and profibrotic genes as well as cardiac fibrosis following chronic MI. Our findings indicate a key protective role for MF-derived miR-150 in modulating post-MI responses.

    DOI: 10.3390/biom14121650

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  • Inducible deletion of microRNA activity in kidney mesenchymal cells exacerbates renal fibrosis

    Hirofumi Sakuma, Keisuke Maruyama, Tatsuya Aonuma, Yuya Kobayashi, Taiki Hayasaka, Kohei Kano, Satoshi Kawaguchi, Kei Ichi Nakajima, Jun Ichi Kawabe, Naoyuki Hasebe, Naoki Nakagawa

    Scientific Reports   14 ( 1 )   2024年12月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41598-024-61560-y

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  • Severe mitral regurgitation in non-hypertrophic cardiomyopathy caused by systolic anterior motion of the mitral valve

    Tatsuya Aonuma, Naoko Kawabata, Ayumi Date, Erika Saito, Kazumi Akasaka, Hiroyuki Kamiya, Naoki Nakagawa

    Journal of Medical Ultrasonics   2024年

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/s10396-024-01480-6

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  • SPRR1A is a key downstream effector of MiR-150 during both maladaptive cardiac remodeling in mice and human cardiac fibroblast activation

    Satoshi Kawaguchi, Bruno Moukette, Marisa N. Sepúlveda, Taiki Hayasaka, Tatsuya Aonuma, Angela K. Haskell, Jessica Mah, Suthat Liangpunsakul, Yaoliang Tang, Simon J. Conway, Il man Kim

    Cell Death and Disease   14 ( 7 )   2023年7月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41419-023-05982-y

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  • Prostaglandin E<inf>2</inf> mediates the late phase of ischemic preconditioning in the heart via its receptor subtype EP<inf>4</inf>

    Takayasu Kanno, Naoki Nakagawa, Tatsuya Aonuma, Jun ichi Kawabe, Koh ichi Yuhki, Naofumi Takehara, Naoyuki Hasebe, Fumitaka Ushikubi

    Heart and Vessels   38 ( 4 )   606 - 613   2023年4月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1007/s00380-022-02219-4

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  • MiR-150 blunts cardiac dysfunction in mice with cardiomyocyte loss of β<inf>1</inf>-adrenergic receptor/β-arrestin signaling and controls a unique transcriptome

    Bruno Moukette, Satoshi Kawaguchi, Marisa N. Sepulveda, Taiki Hayasaka, Tatsuya Aonuma, Suthat Liangpunsakul, Lei Yang, Rohan Dharmakumar, Simon J. Conway, Il man Kim

    Cell Death Discovery   8 ( 1 )   2022年12月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41420-022-01295-9

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  • MiR-150 Attenuates Maladaptive Cardiac Remodeling Mediated by Long Noncoding RNA MIAT and Directly Represses Profibrotic Hoxa4

    Tatsuya Aonuma, Bruno Moukette, Satoshi Kawaguchi, Nipuni P. Barupala, Marisa N. Sepúlveda, Kyle Frick, Yaoliang Tang, Maya Guglin, Subha V. Raman, Chenleng Cai, Suthat Liangpunsakul, Shinichi Nakagawa, Il Man Kim

    Circulation: Heart Failure   15 ( 4 )   E008686   2022年4月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1161/CIRCHEARTFAILURE.121.008686

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  • Sarcopenia-derived exosomal micro-RNA 16-5p disturbs cardio-repair via a pro-apoptotic mechanism in myocardial infarction in mice

    Taiki Hayasaka, Naofumi Takehara, Tatsuya Aonuma, Kohei Kano, Kiwamu Horiuchi, Naoki Nakagawa, Hiroki Tanaka, Jun ichi Kawabe, Naoyuki Hasebe

    Scientific Reports   11 ( 1 )   2021年12月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41598-021-98761-8

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  • Cardiomyocyte microRNA-150 confers cardiac protection and directly represses proapoptotic small proline–rich protein 1A

    Tatsuya Aonuma, Bruno Moukette, Satoshi Kawaguchi, Nipuni P. Barupala, Marisa N. Sepúlveda, Christopher Corr, Yaoliang Tang, Suthat Liangpunsakul, R. Mark Payne, Monte S. Willis, Il Man Kim

    JCI Insight   6 ( 18 )   2021年9月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1172/jci.insight.150405

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  • Interactions between noncoding RNAs as epigenetic regulatory mechanisms in cardiovascular diseases

    Bruno Moukette, Nipuni P. Barupala, Tatsuya Aonuma, Marisa Sepulveda, Satoshi Kawaguchi, Il man Kim

    Methods in Cell Biology   166   309 - 348   2021年1月

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    掲載種別:論文集(書籍)内論文  

    DOI: 10.1016/bs.mcb.2021.06.002

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  • Capillary-resident EphA7<sup>+</sup> pericytes are multipotent cells with anti-ischemic effects through capillary formation

    Yuri Yoshida, Maki Kabara, Kohei Kano, Kiwamu Horiuchi, Taiki Hayasaka, Yui Tomita, Naofumi Takehara, Akiho Minoshima, Tatsuya Aonuma, Keisuke Maruyama, Naoki Nakagawa, Nobuyoshi Azuma, Naoyuki Hasebe, Jun ichi Kawabe

    Stem Cells Translational Medicine   9 ( 1 )   120 - 130   2020年1月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1002/sctm.19-0148

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  • The antioxidant and DNA-repair enzyme apurinic/apyrimidinic endonuclease 1 limits the development of tubulointerstitial fibrosis partly by modulating the immune system

    Keisuke Maruyama, Naoki Nakagawa, Tatsuya Aonuma, Yukihiro Saito, Taiki Hayasaka, Kohei Kano, Kiwamu Horiuchi, Naofumi Takehara, Jun ichi Kawabe, Naoyuki Hasebe

    Scientific Reports   9 ( 1 )   2019年12月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/s41598-019-44241-z

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  • Circular noncoding RNAs as potential therapies and circulating biomarkers for cardiovascular diseases review-article

    Ahmed S. Bayoumi, Tatsuya Aonuma, Jian Peng Teoh, Yao Liang Tang, Il Man Kim

    Acta Pharmacologica Sinica   39 ( 7 )   1100 - 1109   2018年7月

  • β-arrestin-biased agonism of β-adrenergic receptor regulates Dicer-mediated microRNA maturation to promote cardioprotective signaling

    Jian Peng Teoh, Ahmed S. Bayoumi, Tatsuya Aonuma, Yanyan Xu, John A. Johnson, Huabo Su, Neal L. Weintraub, Yaoliang Tang, Il Man Kim

    Journal of Molecular and Cellular Cardiology   118   225 - 236   2018年5月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.yjmcc.2018.04.001

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  • A circular RNA regulator quaking: a novel gold mine to be unfolded in doxorubicin-mediated cardiotoxicity

    Tatsuya Aonuma, Ahmed S. Bayoumi, Yaoliang Tang, Il Man Kim

    Non-Coding RNA Investigation   2   2018年4月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.21037/ncri.2018.04.02

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  • A carvedilol-responsive microRNA, miR-125b-5p protects the heart from acute myocardial infarction by repressing pro-apoptotic bak1 and klf13 in cardiomyocytes

    Ahmed S. Bayoumi, Kyoung mi Park, Yongchao Wang, Jian peng Teoh, Tatsuya Aonuma, Yaoliang Tang, Huabo Su, Neal L. Weintraub, Il man Kim

    Journal of Molecular and Cellular Cardiology   114   72 - 82   2018年1月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.yjmcc.2017.11.003

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  • Pericyte-specific ninjurin1 deletion attenuates vessel maturation and blood flow recovery in hind limb ischemia

    Akiho Minoshima, Maki Kabara, Motoki Matsuki, Yuri Yoshida, Kohei Kano, Yui Tomita, Taiki Hayasaka, Kiwamu Horiuchi, Yukihiro Saito, Tatsuya Aonuma, Masato Nishimura, Keisuke Maruyama, Naoki Nakagawa, Jun Sawada, Naofumi Takehara, Naoyuki Hasebe, Jun Ichi Kawabe

    Arteriosclerosis, Thrombosis, and Vascular Biology   38 ( 10 )   2358 - 2370   2018年

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1161/ATVBAHA.118.311375

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  • MicroRNA-532 protects the heart in acute myocardial infarction, and represses prss23, a positive regulator of endothelial-to-mesenchymal transition

    Ahmed S. Bayoumi, Jian Peng Teoh, Tatsuya Aonuma, Zhize Yuan, Xiaofen Ruan, Yaoliang Tang, Huabo Su, Neal L. Weintraub, Il Man Kim

    Cardiovascular Research   113 ( 13 )   1603 - 1614   2017年11月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1093/cvr/cvx132

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  • Apoptosis-resistant cardiac progenitor cells modified with apurinic/apyrimidinic endonuclease/ redox factor 1 gene overexpression regulate cardiac repair after myocardial infarction

    Tatsuya Aonuma, Naofumi Takehara, Keisuke Maruyama, Maki Kabara, Motoki Matsuki, Atsushi Yamauchi, Jun Ichi Kawabe, Naoyuki Hasebe

    Stem Cells Translational Medicine   5 ( 8 )   1067 - 1078   2016年8月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.5966/sctm.2015-0281

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  • Adult accessory mitral valve with septal hypertrophy

    Tatsuya Aonuma, Naofumi Takehara, Erika Saito, Naoyuki Hasebe

    Internal Medicine   55 ( 17 )   2515   2016年

  • Ninjurin1 is a novel factor to regulate angiogenesis through the function of pericytes

    Motoki Matsuki, Maki Kabara, Yukihiro Saito, Kohei Shimamura, Akiho Minoshima, Masato Nishimura, Tatsuya Aonuma, Naofumi Takehara, Naoyuki Hasebe, Jun Ichi Kawabe

    Circulation Journal   79 ( 6 )   1363 - 1371   2015年5月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1253/circj.CJ-14-1376

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  • Association between microalbuminuria predicting in-stent restenosis after myocardial infarction and cellular senescence of endothelial progenitor cells

    Hisanobu Ota, Naofumi Takehara, Tatsuya Aonuma, Maki Kabara, Motoki Matsuki, Atsushi Yamauchi, Toshiharu Takeuchi, Jun Ichi Kawabe, Naoyuki Hasebe

    PLoS ONE   10 ( 4 )   2015年4月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1371/journal.pone.0123733

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  • Immortalized multipotent pericytes derived from the vasa vasorum in the injured vasculature. A cellular tool for studies of vascular remodeling and regeneration

    Maki Kabara, Jun Ichi Kawabe, Motoki Matsuki, Yoshiki Hira, Akiho Minoshima, Kohei Shimamura, Atsushi Yamauchi, Tatsuya Aonuma, Masato Nishimura, Yukihiro Saito, Naofumi Takehara, Naoyuki Hasebe

    Laboratory Investigation   94 ( 12 )   1340 - 1354   2014年12月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1038/labinvest.2014.121

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  • Nerve growth factor stimulates regeneration of perivascular nerve, and induces the maturation of microvessels around the injured artery

    Akira Asanome, Jun ichi Kawabe, Motoki Matsuki, Maki Kabara, Yoshiki Hira, Hiroki Bochimoto, Atsushi Yamauchi, Tatsuya Aonuma, Naofumi Takehara, Tsuyoshi Watanabe, Naoyuki Hasebe

    Biochemical and Biophysical Research Communications   443 ( 1 )   150 - 155   2014年1月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1016/j.bbrc.2013.11.070

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  • Apurinic/apyrimidinic endonucelase 1 maintains adhesion of endothelial progenitor cells and reduces neointima formation

    Atsushi Yamauchi, Jun Ichi Kawabe, Maki Kabara, Motoki Matsuki, Akira Asanome, Tatsuya Aonuma, Hisanobu Ohta, Naofumi Takehara, Taku Kitagawa, Naoyuki Hasebe

    American Journal of Physiology - Heart and Circulatory Physiology   305 ( 8 )   2013年10月

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    掲載種別:研究論文(学術雑誌)  

    DOI: 10.1152/ajpheart.00965.2012

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▼全件表示

共同研究・競争的資金等の研究課題

  • 抗HER2薬関連心毒性にける新規バイオマーカーlong noncoding RNAの探索

    2024年4月 - 2025年3月

    民間財団等 

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  • 乳癌患者におけるトラスツズマブ関連心毒性の新規バイオマーカーlncRNAの探索

    研究課題/領域番号:22K16060  2022年4月 - 2025年3月

    日本学術振興会  科学研究費助成事業  若手研究

    青沼 達也

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    配分額:4,680,000円 ( 直接経費:3,600,000円 、 間接経費:1,080,000円 )

    アントラサイクリン系抗がん剤としてエピルビシンの治療を受けた後にトラスツズマブ(Trastuzumab:TZB)治療を受けた乳がん患者を対象として症例登録をしているが、本症例の登録基準を満たす患者は半年強で6名と研究開始時の予想を大きく下回った。しかし、少ない症例登録者の中でもアントラサイクリン治療終了時には心臓超音波検査で測定した左室駆出率は59%と左室収縮能が保持されていたが、TZB治療後に左室駆出率が43%まで低下したTZB関連心毒性(+)症例が確認された。同症例ではTZB治療終了時は採血でのトロポニンTやNT-proBNPといった心筋障害や心不全のバイオマーカーの異常はなかったが、TZB関連心毒性(+)としてTZBの一時中断と心保護薬を開始して左室駆出率は改善している。各症例で回収した血漿サンプルは-80℃で保存しており、適宜RNAを抽出して後のlong noncoding RNAアレイ解析に用いる予定である。
    <BR>
    ヒト培養心筋細胞株は当初予定していたAC-16 Human cardiomyocyteではなく、Promo cell社のHuman cardiac myocyte(HCM)を用いて心筋細胞のTZB心毒性を評価する系を構築している。HCMにドキソルビシン(Doxorubicin:DOX)を5-10μMで4時間、次いでTZBを1-10 μMで20時間を投与する系でTUNEL法による細胞のアポトーシス誘導、細胞内ROS産生をそれぞれ評価した。DOXによってHCMのアポトーシス陽性細胞数、細胞内ROSが有意に増加することが確認されたが、DOX後にTZBを投与してアポトーシス陽性細胞、細胞内ROSをDOX単剤より増加させる実験系は未だに確立できていない。反復回数が少なく有意差は示されていないが、定量PCRによる解析ではDOXによる心毒性で上昇すると報告されているlong nocoding RNA MHRTはTZBを投与したHCMで上昇する可能性が示唆された。

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  • 糖尿病循環障害:血流動態的変動指標の確立

    研究課題/領域番号:22K08301  2022年4月 - 2025年3月

    日本学術振興会  科学研究費助成事業  基盤研究(C)

    滝山 由美, 中村 匡徳, 世良 俊博, 青沼 達也

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    配分額:4,160,000円 ( 直接経費:3,200,000円 、 間接経費:960,000円 )

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  • トラスツズマブ関連心毒性におけるlong noncoding RNAの役割に関する検討 英文題目名

    2021年11月

    民間財団等 

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  • IGF-2陽性iPS細胞由来心筋前駆細胞の樹立と 機能解析及び心筋移植効果の検討

    研究課題/領域番号:17K15981  2017年4月 - 2022年3月

    日本学術振興会  科学研究費助成事業  若手研究(B)

    青沼 達也

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    配分額:4,030,000円 ( 直接経費:3,100,000円 、 間接経費:930,000円 )

    本研究の目的は、心筋分化効率が高いiPS細胞由来心筋前駆細胞(iPSC-CPC)を純化、精製してマウス心筋梗塞モデルに移植して治療効果を検討する事である。研究者らの予備検討で心筋分化効率が高い心筋前駆細胞由来iPSCに高発現していたIGF-2に着目し、心筋分化誘導を行ったiPSCからIGF-2陽性細胞を精製した。研究者らは精製したiPSC由来IGF-2陽性細胞は非常に高い心筋分化効率を有する心筋前駆細胞であることが確認し、また精製したIGF-2陽性細胞の拡大培養方法を確立した。

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