Effect of recombinant human annexin A5 on expression of p-PKCα and p120-catenin during endotoxin-induced damage to cardiomyocytes

Abstract

Objective To evaluate the effect of recombinant human annexin A5 on the expression of phosphorylated protein kinase C alpha (p-PKCα) and p120-catenin during endotoxin-induced damage to cardiomyocytes. Methods H9c2 cells cultured in vitro were randomly divided into 3 groups (n=18 each) using a random number table: control group (group C), endotoxin group (group L), and recombinant human annexin A5 group (group A). Recombinant human annexin A5 (final concentration 5 ng/ml) was added, and the cells were incubated for 2 h in group A, and then lipopolysaccharide (final concentration 1 μg/ml) was added, and the cells were incubated for 4 h in L and A groups.At 4 h of incubation, cell apoptosis was detected using the cell apoptosis detection kit, the intercellular space was measured using the confocal microscopy, and the expression of p-PKCα and p120-catenin was determined by Western blot.The apoptosis rate was calculated. Results Compared with group C, the apoptosis rate was significantly increased, the intercellular space was significantly widened, the expression of p120-catenin was significantly down-regulated, and the expression of p-PKCα was significantly up-regulated in group L (P<0.05). Compared with group L, the apoptosis rate and intercellular space were significantly decreased, the expression of p120-catenin was significantly up-regulated, and the expression of p-PKCα was significantly down-regulated in group A (P<0.05). Conclusion Recombinant human annexin A5 can inhibit phosphorylation of PKCα and up-regulate the expression of p120-catenin, thus attenuating endotoxin-induced damage to cardiomyocytes. Key words: Annexin A5; Endotoxins; Myocytes, cardiac; Protein kinase C-alpha; Connexins