RhoA/ROCK pathway regulates hypoxia-induced myocardial cell apoptosis

ABSTRACT

Objective: To observe the regulatory effects of RhoA/ROCK pathway on the apoptosis of cardiac myocyte induced by anoxia and its mechanism. Methods: The model of cardiac myocyte anoxia was established. The beat pulsations and apoptosis rates after 1 h, 3 h, 6 h, 9 h and 12 h of anoxia were recorded and the expressions of RhoA, ROCK1/2, p-PI3K, p-AKT and caspae-3 were detected, too. The apoptosis and the expressions of related proteins were detected after RNAi of RhoA and the inhibition of ROCK by Y-27632. Results: The beat pulsations after 1 h, 3 h, 6 h, 9 h and 12 h decreased gradually but the apoptosis rates increased gradually, and the expressions of RhoA, ROCK1/2, p-PI3K, p-AKT and caspase-3 were increasing along with the increasing duration of anoxia. The apoptotic rates after 1 h, 3 h, 6 h, 9 h and 12 h of anoxia were (4.36[U+4F9D]0.98)%, (8.36[U+4F9D]2.12)%, (15.32[U+4F9D]3.62)%, (18.68[U+4F9D]4.83)% and (24.56[U+4F9D]6.22)%, respectively and decreased more significantly than control group in different time points of anoxia (. P<0.05), and the expressions of RhoA, ROCK1/2, p-PI3K, p-AKT and caspase-3 decreased significantly (. P<0.05). The apoptosis rate and the expressions of RhoA, ROCK1/2, p-PI3K, p-AKT and caspase-3 decreased significantly (. P<0.05) after the inhibition of ROCK by Y-27632 (. P<0.05). Conclusions: RhoA/ROCK pathway plays a critical role in the regulation of the apoptosis of cardiac myocyte induced by anoxia, which may be accompanied by regulating the activity of PI3K/AKT/Caspase-3 pathway.