Uchida, Keiko

写真a

Affiliation

Research Centers and Institutes, Health Center (Hiyoshi)

Position

Associate Professor (Non-tenured)

Career 【 Display / hide

  • 2002.10
    -
    2015.03

    慶應義塾大学, 医学部小児科, 研究員

  • 2010.04
    -
    2015.03

    東京家政学院大学, 現代生活学部健康栄養学科, 准教授

  • 2015.04
    -
    Present

    Keio University, Health Center, Assistant Professor

Academic Background 【 Display / hide

  • 1988.04
    -
    1994.03

    Keio University, 医学部

    Japan, University, Graduated

Academic Degrees 【 Display / hide

  • 博士(医学), Keio University, Dissertation, 2005.12

Licenses and Qualifications 【 Display / hide

  • 医師免許, 1994.05

  • 日本小児科学会小児科専門医, 1998.05

  • 日本小児循環器学会小児循環器専門医, 2015

 

Research Areas 【 Display / hide

  • Pediatrics

  • Developmental biology

  • Cell biology

Research Keywords 【 Display / hide

  • Cardiovascular development

  • Calcium signaling

Research Themes 【 Display / hide

  • Calcium signaling in physiology and pathology, 

    1998.07
    -
    Present

  • Molecular mechanisms of congenital heart diseases, 

    2002.10
    -
    Present

 

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

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

  • Exploring novel proangiogenic factors of pulmonary artery using a LacZ reporter mouse for pulmonary artery smooth muscle

    2020.04
    -
    2023.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 内田 敬子, Grant-in-Aid for Scientific Research (C), Principal Investigator

  • Roles of Tbx4 for Pulmonary Vascular Development and Pulmonary Hypertension

    2017.04
    -
    2020.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 内田 敬子, Grant-in-Aid for Scientific Research (C), Principal Investigator

  • Intracellular Calcium Signals Inhibiting the Progression of Pulmonary Arterial Hypertension

    2014.04
    -
    2017.03

    MEXT,JSPS, Grant-in-Aid for Scientific Research, 内田 敬子, Grant-in-Aid for Scientific Research (C), Principal Investigator

     View Summary

    Inositol trisphosphate receptor (IP3R) is an intracellular Ca2+ release channel. As we found the strong expression of the type 2 IP3R (IP3R2) in the pulmonary arterial smooth muscle cells (PASMCs), we investigated the contribution of IP3R2 to pathophysiology of PAH.
    IP3R2 knockout (KO) mice treated with chronic hypoxia showed higher PA pressure and RV pressure than WT mice in echocardiography. RV hypertrophy and medial wall thickness of PASMCs were more severe in KO. There was significant decrease of TUNEL positive cells in KO, suggesting that apoptosis was reduced in KO PASMCs. Ca2+ imaging revealed that SOCE was enhanced in KO compared with WT. Taken together, chronic hypoxia-induced PAH was deteriorated in IP3R2 KO. The deletion of IP3R2 gene led to inhibition of apoptosis and enhanced SOCE in PASMCs, probably resulting in acceleration of the progression of PAH induced by chronic hypoxia.

 

Courses Taught 【 Display / hide

  • MEDICINE IN MODERN SOCIETY 2

    2020

  • MEDICINE IN MODERN SOCIETY 2

    2019