Reconstitution of intercellular gap junction in transplanted and injured heart
Project/Area Number |
13470148
|
Research Category |
Grant-in-Aid for Scientific Research (B)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Circulatory organs internal medicine
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Research Institution | Osaka Shoin Women's University |
Principal Investigator |
KAZUYA Tsunehiko Osaka Shoin Women's University, Faculty of liberal, professor, 学芸学部, 教授 (80150340)
|
Co-Investigator(Kenkyū-buntansha) |
TOYOFUKU Toshihiko Osaka University, Graduate School of Medicine, Assistant Professor, 医学系研究科, 助手 (60322179)
|
Project Period (FY) |
2001 – 2002
|
Project Status |
Completed (Fiscal Year 2002)
|
Budget Amount *help |
¥14,700,000 (Direct Cost: ¥14,700,000)
Fiscal Year 2002: ¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2001: ¥11,200,000 (Direct Cost: ¥11,200,000)
|
Keywords | Connexin43 / cardiac myocytes / N-cadherin / GATA-4 / semaphorin / gap junction / 筋芽細胞 / 心不全 / wnt蛋白質 / Gap junction / 心筋梗塞 / Wnt蛋白質 |
Research Abstract |
The biological effects of gap and adhesion on cardiac morphogenesis have been investigated. 1.Effects of gap and adhesion molecules on the cell proliferation Connexin43 and N-cadherin suppress the cell proliferation by induction of P21, cell cycle regulator, mediated G2/M arrest. 2.Effects of adhesion molecules on the cardiac morphogenesis Genetically targeted N-cadherin induces the cardia bifida, the failure of single heart formation. The N-cadherin expression is regulated by GATA-4, cardiogenic factor, establishing the biological role of signaling pathway from GATA-54 to N-cadherin. 3.Identification of novel type of semaphorin to regulate cardiac morphogenesis : Semaphorin are originally identified as a regulator for neural development. We identified new member of semaphorin family which regulates cardiac morphogenesis.
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Report
(3 results)
Research Products
(9 results)