Effect Of Guanine Nucleotide Exchange Factor DOCK1on Survival Of Cardiomyocytes

Objectives To observe the effect of guanine nucleotide exchange factorDOCK1on the survival of cardiomyocytes.Methods Rat-derived H9C2cardiomyocytes were transfected witheukaryotic expression recombinant plasmid pCXN2-Flag-hDOCK1(humanDOCK1overexpression plasmid), pCXN2-Flag (empty plasmid) and blank,and treated with hypoxia/reoxygenation (H/R) respectively. Thecardiomyocytes were divided into blank group, empty plasmid group,DOCK1overexpression group, blank+H/R group, empty plasmid+H/Rgroup and DOCK1overexpression+H/R group. The expressions ofDOCK1mRNA and protein were detected by RT-PCR and Western blotrespectively. The changes in actin cytoskeletal reorganization were observedunder confocal laser scanning microscope (CLSM). Apoptosis and cellproliferation rates of the cardiomyocytes were analyzed by flow cytometryand MTT respectively.Results Compared with blank and empty plasimd groups treated witheither H/R or not, human DOCK1mRNA, DOCK1protein and the cell proliferation rate were increased, and the apoptosis rate was decreasedsignificantly in the DOCK1overexpression group treated with either H/R ornot respectively. Compared with DOCK1overexpression group, humanDOCK1mRNA was decreased significantly in the DOCK1overexpression+H/R group. Compared with blank, empty plasmid and DOCK1overexpression groups, rat DOCK1mRNA, DOCK1protein and the cellproliferation rate were decreased, and the apoptosis rate was increasedsignificantly in the blank+H/R, empty plasimd+H/R and DOCK1overexpression+H/R groups respectively (All P <0.05).Conclusions DOCK1can inhibit apoptosis, promote cytoskeletonorderly rearrangement, cell proliferation and survival in the H9C2cardiomyocytes; DOCK1also can inhibit the H/R-induced increase ofapoptosis and decrease of cell proliferation and survival in the H9C2cardiomyocytes.