Effect of guanine nucleotide exchange factor C3G overexpression on survival of cardiomyocytes and its underlying mechanisms
10.3724/SP.J.1008.2012.01172
- Author:
Xu ZHANG
1
Author Information
1. Division of Cardiology, Department of Geriatrics, The First Affiliated Hospital of Chongqing Medical University
- Publication Type:Journal Article
- Keywords:
C3G;
Cardiac myocytes;
Cell survival;
Guanine nucleotide exchange factors
- From:
Academic Journal of Second Military Medical University
2012;33(11):1172-1177
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the effects of the guanine nucleotide exchange factor C3G (Crk SH3-domain-binding guanine-nucleotide-releasing factor) overexpression on the survival of cardiomyocytes and the underlying mechanisms. Methods: H9C2 cardiomyocytes were transiently transfected with pCXN2-Flag or PCXN2-Flag-hC3G (overexposing human C3G mRNA) plasmids, and then were exposed to hypoxia/reoxygenation (H/R) treatment. The cardiomyocytes were divided into blank group, empty plasmid group, C3G overexpression group, blank + H/R group, empty plasmid + H/R group, and C3G overexpression+H/R group. The expression of C3G mRNA was detected by RT-PCR, and the expression of C3G and p-ERK1/2 protein was detected by Western blotting analysis. The apoptosis rates of cardiomyocytes were analyzed by flow cytometry in each group, and the cell proliferation rates were analyzed by MTT. Results: C3G overexpression increased cell proliferation rate and expression of C3G mRNA and protein, p-ERKl protein(all P<0. 01), and decreased apoptosis rate (P< 0. 05,P<0. 01) compared to the blank and empty plasmid groups; the same was true for C3G overexpression+H/R group when compared to the blank+H/R and empty plasmid+H/R groups. Expression of p-ERK2 protein in C3G overexpression+ H/R group was increased compared to blank+H/R and empty plasmid+H/R groups (P< 0. 01). Conclusion: C3G overexpression can promote cell survival in the cardiomyocytes, which might be mediated by the increase of p-ERKl/2 protein expression and apoptosis inhibition.
