MATSUMURA Yoshihiro

写真a

Affiliation

Graduate School of Medicine  Doctorial Course in Medicine  Bioregulatory Medicine  Department of Biochemistry and Metabolic Science

Homepage URL

https://www.med.akita-u.ac.jp/~seika1/en/

Research Interests 【 display / non-display

  • Epigenetics

  • Adipocytes

  • Metabolism

  • Next generation sequencing

  • Histone modifications

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Graduating School 【 display / non-display

  •  
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    1998.03

    Tohoku University     Graduated

Graduate School 【 display / non-display

  •  
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    2004.03

    Tohoku University  Graduate School, Division of Natural Science  Department of Chemistry  Doctor's Course  Completed

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    2001.03

    Tohoku University  Graduate School, Division of Natural Science  Department of Chemistry  Master's Course  Completed

Studying abroad experiences 【 display / non-display

  • 2008.01
    -
    2011.08

    Oregon Health Science University   Postdoctoral researcher

Campus Career 【 display / non-display

  • 2023.11
    -
    Now

    Akita University   Graduate School of Medicine   Doctorial Course in Medicine   Bioregulatory Medicine   Department of Biochemistry and Metabolic Science   Professor  

External Career 【 display / non-display

  • 2022.04
    -
    2023.10

    Tohoku University   Graduate School of Medicine   Associate Professor  

  • 2017.04
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    2022.03

    The University of Tokyo   Research Center for Advanced Science and Technology, Division of Metabolic Medicine   Associate Professor  

  • 2012.04
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    2017.03

    The University of Tokyo   Research Center for Advanced Science and Technology, Division of Metabolic Medicine   Research Associate  

  • 2011.04
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    2012.03

    The University of Tokyo   Research Center for Advanced Science and Technology, Division of Metabolic Medicine   Appointed Research Associate  

  • 2004.06
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    2008.01

    Akita University   Faculty of Medicine   Postdoctoral Researcher  

Research Areas 【 display / non-display

  • Life Science / System genome science  / Epigenetics, Next generation sequencing

  • Life Science / Molecular biology  / Histone modifications, RNA modifications

  • Life Science / Metabolism and endocrinology  / Metabolism, Adipocytes

  • Life Science / Cell biology

  • Life Science / Metabolism and endocrinology

 

Research Achievements 【 display / non-display

    ◆Original paper【 display / non-display

  • Pre-fertilization-origin preservation of brown fat-mediated energy expenditure in humans

    Takeshi Yoneshiro, Mami Matsushita, Sayuri Fuse-Hamaoka, Miyuki Kuroiwa, Yuko Kurosawa, Yosuke Yamada, Makoto Arai, Yuchen Wei, Makoto Iida, Kenichi Kuma, Toshimitsu Kameya, Tomoya Harada, Yoshihiro Matsumura, Tsuyoshi Osawa, Yoshiko Aoki, Hisashi Nakamura, Takafumi Hamaoka, Juro Sakai, Masayuki Saito

    Nature Metabolism     2025.02  [Refereed]

    Research paper (journal)   Domestic Co-author

  • β-Adrenergic Signal and Epigenomic Regulatory Process for Adaptive Thermogenesis

    Yoshihiro Matsumura, Timothy F Osborne, Ryo Ito, Hiroki Takahashi, Juro Sakai

    Advances in Experimental Medicine and Biology ( Springer )  1461   213 - 227   2024.11

    Research paper (journal)   International Co-author

    DOI PubMed

  • Mitochondrial biogenesis in white adipose tissue mediated by JMJD1A-PGC-1 axis limits age-related metabolic disease

    Ito R, Xie S, Tumenjargal M, Sugahara Y, Yang C, Takahashi H, Arai M, Inoue SI, Uchida A, Nakano K, Choi H, Yang G, Zhao Y, Yamaguchi R, Jin H, Sagae H, Wada Y, Tanaka T, Kimura H, Kodama T, Aburatani H, Takeda K, Inagaki T, Osborne TF, Yoneshiro T, Matsumura Y, Sakai J.

    iScience ( iScience )  27 ( 4 ) 109398 - 109398   2024.04  [Refereed]

    Research paper (journal)  

    Mitochondria play a vital role in non-shivering thermogenesis in both brown and subcutaneous white adipose tissues (BAT and scWAT, respectively). However, specific regulatory mechanisms driving mitochondrial function in these tissues have been unclear. Here we demonstrate that prolonged activation of β-adrenergic signaling induces epigenetic modifications in scWAT, specifically targeting the enhancers for the mitochondria master regulator genes Pgc1a/b. This is mediated at least partially through JMJD1A, a histone demethylase that in response to β-adrenergic signals, facilitates H3K9 demethylation of the Pgc1a/b enhancers, promoting mitochondrial biogenesis and the formation of beige adipocytes. Disruption of demethylation activity of JMJD1A in mice impairs activation of Pgc1a/b driven mitochondrial biogenesis and limits scWAT beiging, contributing to reduced energy expenditure, obesity, insulin resistance, and metabolic disorders. Notably, JMJD1A demethylase activity is not required for Pgc1a/b dependent thermogenic capacity of BAT especially during acute cold stress, emphasizing the importance of scWAT thermogenesis in overall energy metabolism.

    DOI PubMed

  • Environmental factor reversibly determines cellular identity through opposing Integrators that unify epigenetic and transcriptional pathways.

    Hiroki Takahashi, Ryo Ito, Yoshihiro Matsumura, Juro Sakai

    BioEssays : news and reviews in molecular, cellular and developmental biology ( BioEssays )  46 ( 2 ) e2300084   2023.11  [Refereed]

    Research paper (journal)   Domestic Co-author

    Organisms must adapt to environmental stresses to ensure their survival and prosperity. Different types of stresses, including thermal, mechanical, and hypoxic stresses, can alter the cellular state that accompanies changes in gene expression but not the cellular identity determined by a chromatin state that remains stable throughout life. Some tissues, such as adipose tissue, demonstrate remarkable plasticity and adaptability in response to environmental cues, enabling reversible cellular identity changes; however, the mechanisms underlying these changes are not well understood. We hypothesized that positive and/or negative "Integrators" sense environmental cues and coordinate the epigenetic and transcriptional pathways required for changes in cellular identity. Adverse environmental factors such as pollution disrupt the coordinated control contributing to disease development. Further research based on this hypothesis will reveal how organisms adapt to fluctuating environmental conditions, such as temperature, extracellular matrix stiffness, oxygen, cytokines, and hormonal cues by changing their cellular identities.

    DOI PubMed

  • Hypoxia activates SREBP2 through Golgi disassembly in bone marrow-derived monocytes for enhanced tumor growth.

    Ryuichi Nakahara, Sho Aki, Maki Sugaya, Haruka Hirose, Miki Kato, Keisuke Maeda, Daichi M Sakamoto, Yasuhiro Kojima, Miyuki Nishida, Ritsuko Ando, Masashi Muramatsu, Melvin Pan, Rika Tsuchida, Yoshihiro Matsumura, Hideyuki Yanai, Hiroshi Takano, Ryoji Yao, Shinsuke Sando, Masabumi Shibuya, Juro Sakai, Tatsuhiko Kodama, Hiroyasu Kidoya, Teppei Shimamura, Tsuyoshi Osawa

    The EMBO journal ( EMBO Journal )  42 ( 22 ) e114032   2023.10  [Refereed]

    Research paper (journal)   Domestic Co-author

    Bone marrow-derived cells (BMDCs) infiltrate hypoxic tumors at a pre-angiogenic state and differentiate into mature macrophages, thereby inducing pro-tumorigenic immunity. A critical factor regulating this differentiation is activation of SREBP2-a well-known transcription factor participating in tumorigenesis progression-through unknown cellular mechanisms. Here, we show that hypoxia-induced Golgi disassembly and Golgi-ER fusion in monocytic myeloid cells result in nuclear translocation and activation of SREBP2 in a SCAP-independent manner. Notably, hypoxia-induced SREBP2 activation was only observed in an immature lineage of bone marrow-derived cells. Single-cell RNA-seq analysis revealed that SREBP2-mediated cholesterol biosynthesis was upregulated in HSCs and monocytes but not in macrophages in the hypoxic bone marrow niche. Moreover, inhibition of cholesterol biosynthesis impaired tumor growth through suppression of pro-tumorigenic immunity and angiogenesis. Thus, our findings indicate that Golgi-ER fusion regulates SREBP2-mediated metabolic alteration in lineage-specific BMDCs under hypoxia for tumor progression.

    DOI PubMed

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    ◆Other【 display / non-display

  • Multi-omics in lifestyle-related diseases

    実験医学   41 ( 15 )   2023

    Domestic Co-author

    J-GLOBAL

  • Mechanisms of Adipocyte Fate Determination Through Epigenetic Changes in Response to Environmental Fluctuations.

    Bio Industry   40 ( 5 )   2023

    J-GLOBAL

  • 脂肪生成中におけるヒストン脱メチル化酵素KDM4Cを用いた遺伝子座特異的エピゲノム編集(Locus-specific epigenome editing using histone demethylase KDM4C during adioogenesis)

    澤田 知伸, 松村 欣宏, 植木 浩二郎, 門脇 孝, 酒井 寿郎

    肥満研究 ( (一社)日本肥満学会 )  23 ( Suppl. ) 204 - 204   2017.09

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Grant-in-Aid for Scientific Research 【 display / non-display

  • A Study on Elucidating Obesity and Lifestyle Diseases through the Epigenome-RNA Modification Axis

    Grant-in-Aid for Scientific Research(S)

    Project Year: 2024.04  -  2029.03 

  • Grant-in-Aid for Challenging Research (Pioneering)/(Exploratory)

    Project Year: 2022.06  -  2026.03 

  • Elucidation of epigenome dynamics that determines adipocyte differentiation

    Grant-in-Aid for Scientific Research(C)

    Project Year: 2022.04  -  2025.03 

  • Grant-in-Aid for Scientific Research(A)

    Project Year: 2021.04  -  2024.03 

  • Elucidation of epigenetic mechanisms that memorize inter-tissue communication

    Grant-in-Aid for Scientific Research(C)

    Project Year: 2019.04  -  2022.03  Investigator(s): Matsumura Yoshihiro

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Presentations 【 display / non-display

  • JMJD1Aは脂肪細胞分化においてグルコース代謝と脂質貯蔵を促進する

    楊晨旭,Eko Fuji Ariyanto,張吉,伊藤亮,謝詩雨,米代武司,稲垣毅,曽我朋義,松村欣宏,酒井寿郎

    第97回日本生化学会大会  (横浜)  2024.11  -  2024.11 

  • Glucose-sensing JMJD1A facilitates glucose metabolism and lipid storage during adipogenesis

    楊晨旭,Eko Fuji Ariyanto,張吉,伊藤亮,謝詩雨,米代武司,稲垣毅,曽我朋義,松村欣宏,酒井寿郎

    第45回日本肥満学会 第42回日本肥満症治療学会学術集会  (横浜)  2024.10  -  2024.10 

  • Mitochondrial Biogenesis in White Adipose Tissue Mediated by JMJD1APGC-1 Axis Limits Age-related Metabolic Disease

    謝詩雨,伊藤亮,Myagmar Tumenjargal,米代武司,松村欣宏,酒井寿郎

    第42回内分泌代謝学サマーセミナー  (群馬)  2024.07  -  2024.07 

  • Glucose-sensing JMJD1A facilitates glucose metabolism and lipid storage during adipogenesis

    楊晨旭,Eko Fuji Ariyanto,張吉,伊藤亮,謝詩雨,米代武司,稲垣毅,曽我朋義,松村欣宏,酒井寿郎

    第42回内分泌代謝学サマーセミナー  (群馬)  2024.07  -  2024.07