| 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)
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| 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.
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