Hasuwa, Hidetoshi

写真a

Affiliation

School of Medicine, Center for the Promotion of Interdiciplinary Research in Medicine and Life Scieince(Research Centers, Laboratory of Developmental Engineering) ( Shinanomachi )

Position

Assistant Professor/Senior Assistant Professor

External Links
Scopus Paper Info  
Paper Count: 45 Citation Count: 3868 h-index: 25

Click to view the Scopus page. The data was downloaded from Scopus API in July 19, 2026, via http://api.elsevier.com and http://www.scopus.com .

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Academic Degrees 【 Display / hide 】

  • 博士（医学）, 久留米大学, Coursework

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Research Areas 【 Display / hide 】

  • Life Science / Laboratory animal science

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Research Keywords 【 Display / hide 】

  • 遺伝子改変動物・非コードRNA

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Papers 【 Display / hide 】

  • GPAT2 is required for piRNA biogenesis, transposon silencing, and maintenance of spermatogonia in mice†

    Shiromoto Y., Kuramochi-Miyagawa S., Nagamori I., Chuma S., Arakawa T., Nishimura T., Hasuwa H., Tachibana T., Ikawa M., Nakano T.

    Biology of reproduction (Biology of reproduction)  101 ( 1 ) 248 - 256 2019.07

    　View Summary

    © The Author(s) 2019. Published by Oxford University Press on behalf of Society for the Study of Reproduction. PIWI-interacting RNAs (piRNAs), a subclass of germ cell-specific noncoding small RNAs, are essential for de novo DNA methylation of retrotransposon genes in embryonic testes. PIWIL2/MILI, one of three mouse PIWI family members, is indispensable for piRNA production, DNA methylation of retrotransposons presumably via piRNA, and normal spermatogenesis. In vitro analysis using germline stem cells (GS cells) revealed that glycerol-3-phosphate acyltransferase 2 (GPAT2), which is a mitochondrial outer membrane protein involved in generation of lysophosphatidic acid (LPA) and highly expressed in testes, plays important roles in spermatogenesis. Namely, GPAT2 binds to PIWIL2 and is closely involved in the biogenesis of piRNAs; this process is independent of its enzymatic activity on LPA. However, GS cells recapitulate only a limited phase of spermatogenesis and the biological functions of GPAT2 remain largely unknown. In this study, we generated GPAT2-deficient mice and conducted comprehensive analyses. The deficient mice showed defective piRNA production and subsequent de-silencing of IAP and Line-1 retrotransposons in fetal testes. In addition, apoptosis of pachytene spermatocytes was observed. These abnormalities were all common to the phenotype of PIWIL2-deficient mice, in which piRNA production was impaired. GPAT2-deficient mice exhibited apoptosis in spermatogonia at the neonatal stage, which was not observed in PIWIL2-deficient mice. These data show that GPAT2 plays a critical role in preventing apoptosis in spermatogonia.

  • Female mice lacking Ftx lncRNA exhibit impaired X-chromosome inactivation and a microphthalmia-like phenotype

    Hosoi Y., Soma M., Shiura H., Sado T., Hasuwa H., Abe K., Kohda T., Ishino F., Kobayashi S.

    Nature Communications (Nature Communications)  9 ( 1 )  2018.12

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    © 2018, The Author(s). X-chromosome inactivation (XCI) is an essential epigenetic process in female mammalian development. Although cell-based studies suggest the potential importance of the Ftx long non-protein-coding RNA (lncRNA) in XCI, its physiological roles in vivo remain unclear. Here we show that targeted deletion of X-linked mouse Ftx lncRNA causes eye abnormalities resembling human microphthalmia in a subset of females but rarely in males. This inheritance pattern cannot be explained by X-linked dominant or recessive inheritance, where males typically show a more severe phenotype than females. In Ftx-deficient mice, some X-linked genes remain active on the inactive X, suggesting that defects in random XCI in somatic cells cause a substantially female-specific phenotype. The expression level of Xist, a master regulator of XCI, is diminished in females homozygous or heterozygous for Ftx deficiency. We propose that loss-of-Ftx lncRNA abolishes gene silencing on the inactive X chromosome, leading to a female microphthalmia-like phenotype.

  • Vwf K1362A resulted in failure of protein synthesis in mice

    Sanda N., Suzuki N., Suzuki A., Kanematsu T., Kishimoto M., Hasuwa H., Takagi A., Kojima T., Matsushita T., Nakamura S.

    International Journal of Hematology (International Journal of Hematology)  107 ( 4 ) 428 - 435 2018.04

    ISSN  09255710

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    © 2018, The Japanese Society of Hematology. Von Willebrand factor (VWF) is synthesized in megakaryocytes and endothelial cells (ECs) and has two main roles: to carry and protect coagulation factor VIII (FVIII) from degradation by forming VWF–FVIII complex; and to mediate platelet adhesion and aggregation at sites of vascular injury. Previous research using the HEK293 cell line revealed that the VWF K1362 mutation interacted directly with platelet glycoprotein Ib (GPIb). Vwf K1362A knock-in (KI) mice were therefore generated to verify the in vivo function of residue 1362 in binding to platelet GPIb. The Cre-loxP system was employed to introduce the Vwf K1362A mutation systemically in mice. In blood coagulation analysis, the VWF antigen (VWF:Ag) of Lys1362Ala KI homozygous (homo) mice was below the sensitivity of detection by enzyme-linked immunosorbent assay. FVIII activities (FVIII:C) were 47.9 ± 0.3 and 3.3 ± 0.3% (K1362A heterozygous (hetero) and K1362A KI homo mice, respectively) compared to wild-type mice. Immunohistochemical staining analysis revealed that VWF protein did not exist in ECs of K1362A KI homo mice. These results indicated that VWF protein synthesis of K1362A was impaired after transcription in mice. K1362 seems to represent a very important position not only for VWF function, but also for VWF synthesis in mice.

  • Human PIWI (HIWI) is an azoospermia factor

    Hasuwa H., Ishino K., Siomi H.

    Science China Life Sciences (Science China Life Sciences)  61 ( 3 ) 348 - 350 2018.03

    ISSN  16747305

  • Constitutive overexpression of periostin delays wound healing in mouse skin

    Nunomura S., Nanri Y., Ogawa M., Arima K., Mitamura Y., Yoshihara T., Hasuwa H., Conway S., Izuhara K.

    Wound Repair and Regeneration (Wound Repair and Regeneration)  26 ( 1 ) 6 - 15 2018.01

    ISSN  10671927

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    © 2018 by the Wound Healing Society Periostin is a matricellular protein involved in development, maintenance, and regulation of tissues and organs via by binding to cell surface integrin receptors. Pathologically, periostin plays an important role in the process of wound healing: as a deficiency of the Postn gene delays wound closure and periostin is consistently up-regulated in response to injury and skin diseases. However, the functional role of elevated periostin in the process of wound healing has not been tested. In this study, we generated Postn-transgenic mice under the control of the CAG promoter/enhancer to investigate the effects of constitutive overexpression of full length periostin during its pathophysiological roles. Transgenic mice showed significant overexpression of periostin in skin, lung, and heart, but no morphological changes were observed. However, when these transgenic mice were injured, periostin overexpression delayed the closure of excisional wounds. Expression of IL-1β and TNFα, pro-inflammatory cytokines important for wound healing, was significantly decreased in the transgenic mice, prior to delayed healing. Infiltration of neutrophils and macrophages, the main sources of IL-1β and TNFα, was also down-regulated in the transgenic wound sites. From these data, we conclude that enforced expression of periostin delays wound closure due to reduced infiltration of neutrophils and macrophages followed by down-regulation of IL-1β and TNFα expression. This suggests that regulated spatiotemporal expression of periostin is important for efficient wound healing and that constitutive periostin overexpression interrupts the normal process of wound closure.

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Papers, etc., Registered in KOARA 【 Display / hide 】

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Reviews, Commentaries, etc. 【 Display / hide 】

  • Publisher Correction: Female mice lacking Ftx lncRNA exhibit impaired X-chromosome inactivation and a microphthalmia-like phenotype (Nature Communications, (2018), 9, 1, (3829), 10.1038/s41467-018-06327-6)

    Hosoi Y., Soma M., Shiura H., Sado T., Hasuwa H., Abe K., Kohda T., Ishino F., Kobayashi S.

    Nature Communications (Nature Communications)  9 ( 1 )  2018.12

    　View Summary

    © 2018, The Author(s). Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan; Technology and Development Team for Mammalian Genome Dynamics, RIKEN BioResource Research Center, 3-1-1 Koyadai, Tsukuba, Ibaraki, 305-0074, Japan; Present address: Faculty of Life and Environmental Sciences, University of Yamanashi, 4-4-37 Takeda, Kofu, Yamanashi, 400-8510, Japan’. The correct affiliations are: ‘Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo 113-8510, Japan; Technology and Development Team for Mammalian Genome Dynamics, RIKEN BioResource Research Center, 3-1-1 Koyadai, Tsukuba, Ibaraki 305-0074, Japan; Faculty of Life and Environmental Sciences, University of Yamanashi, 4-4-37 Takeda, Kofu, Yamanashi 400-8510, Japan’. Also, in the original HTML version of this Article, the affiliation details for Hidetoshi Hasuwa were incorrectly given as: ‘Research Institute for Microbial Diseases, Osaka University, Yamadaoka 3-1, Suita, Osaka, 565-0871, Japan’. The correct affiliations are: ‘Research Institute for Microbial Diseases, Osaka University, Yamadaoka 3-1, Suita, Osaka, 565-0871, Japan; Present address: Department of Molecular Biology, Keio University School of Medicine, Tokyo, 160-8582, Japan’. Additionally, in the original HTML version of this Article, the affiliation details for Takashi Kohda were incorrectly given as: ‘Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan; Present address: Department of Molecular Biology, Keio University School of Medicine, Tokyo, 160-8582, Japan’. The correct affiliations are: ‘Department of Epigenetics, Medical Research Institute, Tokyo Medical and Dental University (TMDU), 1-5-45 Yushima, Bunkyo-ku, Tokyo, 113-8510, Japan; Faculty of Life and Environmental Sciences, University of Yamanashi, 4-4-37 Takeda, Kofu, Yamanashi 400-8510, Japan’.

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Research Projects of Competitive Funds, etc. 【 Display / hide 】

  • 遺伝子改変ゴールデンハムスターを用いた初期胚発生に保存された生命現象の解明

    2025.04
    -
    2030.03

    基盤研究(B), Principal investigator

  • トランスジェニックゴールデンハムスターの作製と精子凍結保存法の開発

    2023.06
    -
    2026.03

    挑戦的研究（萌芽）, Principal investigator

  • ハムスターをモデルとした卵形成時におけるレトロトランスポゾン制御機構の解明

    2020.04
    -
    2023.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, Grant-in-Aid for Scientific Research (B), Principal investigator

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Courses Taught 【 Display / hide 】

  • COORDINATED CURRICULUM ON BEING A PROFESSIONAL STUDENT IN MEDICAL SCIENCES

    2026

  • BASIC ONCOLOGY

    2026

  • MEDICAL PROFESSIONALISM 3

    2026

  • MEDICAL SCIENCE METHODOLOGY

    2026

  • MOLECULAR BIOLOGY

    2026

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