Role of gap-junctional coupling between cardiomyocytes and stromal cells in genesis of cardiac arrhythmias
Project/Area Number |
21590420
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Single-year Grants |
Section | 一般 |
Research Field |
Experimental pathology
|
Research Institution | Kyoto Prefectural University of Medicine |
Principal Investigator |
TANAKA Hideo 京都府立医科大学, 大学院・医学研究科, 准教授 (60236619)
|
Project Period (FY) |
2009 – 2011
|
Project Status |
Completed (Fiscal Year 2011)
|
Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2009: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
|
Keywords | 線維芽細胞 / 心筋梗塞 / ギャップ結合 / 不整脈 / 肉芽組織 / 間質 / 心筋 / 梗塞 |
Research Abstract |
During the healing phase of myocardial infarct, proliferation of endothelial cells and fibroblasts constitute granulation tissue to replace the infarct resion. Recent reports have confirmed that stromal cells, especially fibroblasts, coupled electrically with cardiomyocytes via gap junction proteins connexins, provide an important basis for cardiac arrhythmias.However, it is unresoloved whether or not stromal cells at the border zone of myocardial infarct really contribute to the arrhythmogenesis. To address this, this project was conducted by using an infarct model of conditional knockout mice specific for Cx43 in the Fsp-1 proteins. Continuous ECG recording in combination with histological analysis was conducted in the Fsp-Cre/Cx43 loxP mice. It was found that the heart devoid of Cx43 in the fibroblasts and endothelial cells failed to attenuate ventricular arrhythmias after infarction. However, formation of granulation tissue showed a significant retardation in the Cx43-KO mice after infarction as compared with wild type mice. The results indicate that Cx43 contributes to formation of granulation tissue in the infarct heart.
|
Report
(4 results)
Research Products
(28 results)
-
-
[Journal Article] promotes cardiac dysfunction in diabetic mellitus due to excessive mitochondrial respiration-mediated ROS generation and lipid accumulation Circ- Heart Fail2012
Author(s)
Nakamura H, Matoba S, Iwai-Kanai E, Kimata M, Hoshino A, Nakaoka M, Katamura M, Okawa Y, Mita Y, Ikeda K, Okigaki M, Adachi S, Tanaka H, Takamatsu T, Matsubara H
-
Journal Title
Eur Heart J.
Volume: 5巻
Issue: 1
Pages: 106-115
DOI
Related Report
Peer Reviewed
-
-
[Journal Article] p53 promotes cardiac dysfunction in diabetic mellitus due to excessive mitochondrial respiration-mediated ROS generation and lipid accumulation2012
Author(s)
Nakamura H, Matoba S, Iwai-Kanai E, Kimata M, Hoshino A, Nakaoka M, Katamura M, Okawa Y, Mita Y, Ikeda K, Okigaki M, Adachi S, Tanaka H, Takamatsu T, Matsubara H
-
Journal Title
Circ-Heart Fail
Volume: 5
Pages: 106-115
Related Report
Peer Reviewed
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-