Effct Of Dock180Silence On Hypoxia/Reoxygenation Induced Apoptosis And Survival Inhibition In Cardiomyocytes And Its Underlying Mechanism

Objectives: To investigate the effect of Dock180silence onhypoxia/reoxygenation (H/R) induced apoptosis and survival inhibition incardiomyocytes and its underlying mechanisms.Methods: H9C2cardiomyocytes were infected with blank，negativelentivirus and Dock180RNAi lentivirus (Dock180mRNA silence)，thentreated with H/R respectively. The cardiomyocytes were divided into blankgroup, negative lentivirus group, Dock180silence group, blank+H/R group,negative lentivirus+H/R group and Dock180silence+H/R group. Theexpression of Dock180mRNA was detected by RT-PCR, and the expressionof Dock180and p-ERK1/2protein was detected by Western blottinganalysis. Apoptosis rate of cardiomyocytes was analyzed by flow cytometry（FCM）, and the cell proliferation rate was analyzed by MTT. The changeof F-actin cytoskeleton was observed under confocal laser scanningmicroscope (CLSM).Results: Compared with blank&negative lentivirus groups and blank+H/R&negative lentivirus+H/R groups, Dock180mRNA&protein、p-ERK1protein、 p-ERK2protein and proliferation rate were significantly decreased(p<0.01), apoptosis rate was significantly increased(p<0.01,p<0.05)，and the F-actin cytoskeleton was more disorderly in the Dock180silence and Dock180silence+H/R groups respectively.Conclusions: Dock180silence can enhance H/R induced apoptosis andsurvival inhibition in cardiomyocytes, which might be mediated by thedecrease of p-ERK1/2protein expression.