YASUI Masato

写真a

Affiliation

School of Medicine, Department of Pharmacology ( Shinanomachi )

Position

Professor

Related Websites
Scopus Paper Info  
Paper Count: 180 Citation Count: 7470 h-index: 43

Click to view the Scopus page. The data was downloaded from Scopus API in May 17, 2026, via http://api.elsevier.com and http://www.scopus.com .

Page Top ▲

Other Affiliation 【 Display / hide 】

  • School of Medicine, Professor

Page Top ▲

Career 【 Display / hide 】

  • 1989.04
    -
    1992.03

    St. Luke’s International Hospital, Pediatrics, Clinical Resident

  • 1992.04
    -
    1993.01

    Tokyo Women’s Medical University, Neonatolgy, Clinical Fellow

  • 1992.04
    -
    1993.01

    University of Tokyo, Dept. of Molecular Neurobiology, Guest Researcher

  • 2000
    -
    2001

    Johns Hopkins School of Medicine, Instructor

  • 2001
    -
    2006

    Johns Hopkins School of Medicine, USA, Depts of Pediatrics and Biological Chemistry, Assistant Professor

display all >>

Page Top ▲

Academic Background 【 Display / hide 】

  • 1983.04
    -
    1989.03

    Keio University, School of Medicine

    University, Graduated

  • 1997.04

    the Karolinska Institute (Stockholm, Sweden), Doctor of Philosophy (Ph. D.)

    Sweden, Graduate School, Graduated, Doctoral course

Page Top ▲

Academic Degrees 【 Display / hide 】

  • Doctor of Philosophy, スウェーデン王国カロリンスカ医科大学, 1997.04

  • 博士(医学）, 慶応義塾大学, 1998

Page Top ▲

Licenses and Qualifications 【 Display / hide 】

  • Medical License, 1989.05

Page Top ▲
 

Research Areas 【 Display / hide 】

  • Life Science / Pharmacology

Page Top ▲

Research Keywords 【 Display / hide 】

  • 水・電解質・アクアポリン

Page Top ▲

Research Themes 【 Display / hide 】

  • ①アクアポリンの構造機能相関　②脳のアクアポリンの機能解析　③アクアフォトミクスの臨床応用, 

    1997.01
    -
    Present

Page Top ▲
 

Papers 【 Display / hide 】

  • Aquaporin 3 inhibition attenuates imiquimod-induced psoriatic symptoms in a murine model

    Okubo R., Tanaka M., Kubo A., Yasui M., Hara-Chikuma M.

    Molecular Biology Reports 52 ( 1 )  2025.12

    ISSN  03014851

    　View Summary

    Background: Aquaporin 3 (AQP3) is highly expressed in both keratinocytes and T cells within psoriatic skin. Previous studies have demonstrated that AQP3 knockout mice show reduced development of psoriatic symptoms in murine models. This study aims to evaluate the effect of AQP3 inhibition on psoriasis progression. Methods and results: AQP3 conditional knockout mice were generated to assess the role of AQP3 expression in keratinocytes and T cells in psoriasis pathogenesis. In an imiquimod (IMQ)-induced psoriasis model, psoriatic symptoms were significantly reduced in mice with keratinocyte-specific AQP3 deletion. Additionally, AQP3 inhibition by administration of anti-AQP3 monoclonal antibody (mAb) effectively alleviated IMQ-induced psoriasis symptoms in wild-type mice. Conclusions: AQP3 inhibition presents a promising approach for the treatment of psoriasis.

  • Early neuromyelitis optica antibody-induced molecular changes in aquaporin 4 and associated proteins at astrocyte endfeet in murine brain tissues

    Yoshikawa Y., Tomioka M., Abe Y., Yasui M., Nuriya M.

    Journal of Pharmacological Sciences 158 ( 3 ) 212 - 218 2025.07

    ISSN  13478613

    　View Summary

    Neuromyelitis optica spectrum disorder (NMOSD) is characterized by the production of autoantibodies against aquaporin 4 (AQP4). Because NMOSD progressively causes irreversible and severe neurological damages, understanding the initial molecular changes induced by anti-AQP4 antibody binding is crucial for designing early interventions. However, knowledge about the effects of the antibodies before AQP4 loss in brain tissues is limited. Using acutely prepared mouse brain slices, we aimed to investigate the initial molecular impact of NMO model antibodies on AQP4 and its associated proteins. We employed two different types of NMO model antibodies, E5415A and E5415B; E5415A recognizes both M1 and M23 isoforms, whereas E5415B exclusively binds to M23. We found that E5415A but not E5415B disrupted the uniform perivascular localization of AQP4, leading to fragmentation. We further addressed the impact of these changes on AQP4-associated proteins and found that strong colocalizations between AQP4 and dystrophin-glycoprotein complex (DGC) components were preserved, even after AQP4 localization pattern became fragmented. Thus, our study reveals the initial molecular changes in the AQP4 channel at the astrocytic endfeet in response to NMO model antibodies and highlights the early pathological events occurring in NMOSD.

  • Cooling-rate dependence of the cryopreservation of aquaporin-overexpressing cells with a non-permeable cryoprotectant

    Matsuo S., Yamazaki K., Yasui M., Abe Y., Uchida T.

    Cryobiology 119 2025.06

    ISSN  00112240

    　View Summary

    Dehydration of intracellular water is an important factor in the cryopreservation of cells, but questions remain as to the appropriate amount and timing of dehydration and the detailed mechanism of the freezing process. Answering these questions will lead to improvements in cryopreservation methods that have remained unchanged for more than half a century and to an increase in the number of cell types that can be cryopreserved. Therefore, we aimed to reveal the time point when cells were dehydrated in their cooling process and how much their viabilities were improved by dehydration. We conducted cryopreservation experiments using cells with enhanced water permeability due to membrane overexpression of the water transport channel protein (AQP4). The AQP4-expressing cells or non-AQP4-expressing cells were cryopreserved under different cooling rates after addition of the membrane-permeable cryoprotectant (CPA) Me<inf>2</inf>SO, the non-membrane-permeable CPA trehalose, or no CPA. The results showed that no cryopreservation was successful without CPAs, even in the AQP4-expressing cells with increased water permeability. At slow freezing rates below 35 °C/min, viability with Me<inf>2</inf>SO was maintained with decreasing in the cooling rate, but with trehalose, the viability decreased. At cooling rates above 80 °C/min, the viability of AQP4-expressing cells was significantly higher than that of AQP4-non-expressing cells. These results suggest that dehydration due to the osmotic-pressure difference generated after extracellular freezing is fatal to cells.

  • Title: Identification of Redox State Based on the Difference in Solvation Dynamics

    Kato Y., Muncan J., Hirano Y., Yamamoto H., Tsenkova R., Yasui M.

    Chemistryopen 14 ( 5 )  2025.05

    　View Summary

    Oxidation-reduction (Redox) reactions are crucial for many biological processes, yet there is no method available to evaluate redox states in a non-invasive, continuous manner. Here we introduce a novel approach to distinguish between reduced and oxidized states of glutathione (GSH and GSSG, respectively) using aquaphotomics near-infrared (NIR) spectroscopy and multivariate analysis. We identified clear differences in NIR spectra reflecting not only glutathione itself, but different redox states of glutathione based on the spectral features of water molecular conformations interacting with the reaction site. Molecular dynamic simulations also revealed the difference in water molecule coordination and hydration numbers around the reaction site. This approach not only sheds light on the significance of water molecules in redox reactions but also enables non-destructive, continuous assessment of redox states, with potential applications for bioreactor optimization.

  • HSP90 promotes tumor associated macrophage differentiation during triple-negative breast cancer progression

    Hong L., Tanaka M., Yasui M., Hara-Chikuma M.

    Scientific Reports 14 ( 1 )  2024.12

    　View Summary

    Tumor-associated macrophages (TAMs) originating from monocytes are crucial for cancer progression; however, the mechanism of TAM differentiation is unclear. We investigated factors involved in the differentiation of monocytes into TAMs within the tumor microenvironment of triple-negative breast cancer (TNBC). We screened 172 compounds and found that a heat shock protein 90 (HSP90) inhibitor blocked TNBC-induced monocyte-to-TAM differentiation in human monocytes THP-1. TNBC-derived conditional medium (CM) activated cell signaling pathways, including MAP kinase, AKT and STAT3, and increased the expression of TAM-related genes and proteins. These inductions were suppressed by HSP90 inhibition or by knockdown of HSP90 in TNBC. Additionally, we confirmed that TNBC secreted HSP90 extracellularly and that HSP90 itself promoted TAM differentiation. In a mouse tumor model, treatment with an HSP90 inhibitor suppressed tumor growth and reduced TAMs in the tumor microenvironment. Our findings demonstrate the role of HSP90 in TAM differentiation, suggesting HSP90 as a potential target for TNBC immunotherapy due to its regulatory role in monocyte-to-TAM differentiation.

display all >>

Page Top ▲

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

display all >>

Page Top ▲

Presentations 【 Display / hide 】

  • Roles of aquaporin‐ 4(AQP4)in neurodegenerative diseases

    Third Annual Stanford/Kanagawa Symposium, 

    2018.11

  • 睡眠研究の最先端―ストレス社会で健康を守るために

    在ベルリン日本大使館慶應義塾大学医学講演会, 

    2018.10

  • アクアポリン４（AQP4）と神経変性疾患の病態生理

    [Domestic presentation]  第30回日本神経免疫学会学術集会, 

    2018.09

  • New Insight into Aquaporin Function as Drug Targets

    [International presentation]  18th World Congress of Basic and Clinical Pharmacology, 

    2018.07

  • 脳のアクアポリンと神経変性疾患

    [Domestic presentation]  第30回臨床MR脳機能研究会学術集会, 

    2018.04

display all >>

Page Top ▲

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

  • 脳リンパ流の生理とその破綻による高次脳機能低下メカニズムの解明

    2018.04
    -
    2021.03

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

  • Development of a new therapy for brain edema: study for regulation of AQP4 as a molecular target

    2015.04
    -
    2018.03

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

Page Top ▲
 

Courses Taught 【 Display / hide 】

  • PHARMACOLOGY: PRACTICE

    2026

  • STRUCTURAL BIOLOGY: SEMINAR

    2026

  • STRUCTURAL BIOLOGY: PRACTICE

    2026

  • ADVANCED PHARMACOLOGY

    2026

  • PHARMACOLOGY: SEMINAR

    2026

display all >>

Page Top ▲

Courses Previously Taught 【 Display / hide 】

  • 薬理学総論・薬理学各論・薬理学実習

    Keio University

    2017.04
    -
    2018.03

  • 薬理学総論・薬理学各論・薬理学実習

    Keio University

    2015.04
    -
    2016.03
    , 

    Spring Semester

Page Top ▲

Educational Activities and Special Notes 【 Display / hide 】

  • NEW薬理学

    1989.02

    , Development of Textbook and Teaching Material

Page Top ▲
 

Memberships in Academic Societies 【 Display / hide 】

  • 日本薬理学会・日本小児科学会・日本臨床薬理学会・日本生物物理学会

    　
Page Top ▲