Objective: To study in vitro the role of cytoskeleton in the mechanisms of stretch-induced cardiomyocyte hypertrophy. Methods: After cultured on a deformable membrane, the myocardial cells were incorporated with 3H-le...Objective: To study in vitro the role of cytoskeleton in the mechanisms of stretch-induced cardiomyocyte hypertrophy. Methods: After cultured on a deformable membrane, the myocardial cells were incorporated with 3H-leucine (3H-leu) to determine the hypertrophic rate. The contents of angiotensin II and endothelin in the supernatant of the culture medium were measured with radioimmunoassay. Results: Colchicine at 4 μmol/L partially inhibited 3H-leu incorporation rate of the stretch-induced cardiomyocytes but cytochalasin B showed no such effect. The radioactivity of 3H-leu incorporation in the supernatant of the culture medium was significantly lower in the cardiomyocyte culture treated with colchicines (μmol/L) or cytochalasin (0.4μmol/L) than in simple myocardial cell culture. In addition, the 2 agents markedly inhibited the myocardial cells from secreting angiotensin II and endothin. Conclusion: The cytoskeleton plays a role in the stretch-induced mycardiocyte hypertrophy by mediating the secretion of the cell growth factors by the cells themselves.展开更多
基金National Natural Science Foundation of ChinaNo. 39600041)
文摘Objective: To study in vitro the role of cytoskeleton in the mechanisms of stretch-induced cardiomyocyte hypertrophy. Methods: After cultured on a deformable membrane, the myocardial cells were incorporated with 3H-leucine (3H-leu) to determine the hypertrophic rate. The contents of angiotensin II and endothelin in the supernatant of the culture medium were measured with radioimmunoassay. Results: Colchicine at 4 μmol/L partially inhibited 3H-leu incorporation rate of the stretch-induced cardiomyocytes but cytochalasin B showed no such effect. The radioactivity of 3H-leu incorporation in the supernatant of the culture medium was significantly lower in the cardiomyocyte culture treated with colchicines (μmol/L) or cytochalasin (0.4μmol/L) than in simple myocardial cell culture. In addition, the 2 agents markedly inhibited the myocardial cells from secreting angiotensin II and endothin. Conclusion: The cytoskeleton plays a role in the stretch-induced mycardiocyte hypertrophy by mediating the secretion of the cell growth factors by the cells themselves.
