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- Title
C3 G overexpression promotes the survival of rat-derived H9 C2 cardiomyocytes by p-ERK1/2.
- Authors
Zhang, Xu; Li, Gang; Zhang, Lei; Yang, Dongyan; Zhang, Zhisheng; Yan, An; Linghu, Hua
- Abstract
Integrin β1 subunit and its downstream molecules, such as integrin-linked kinase and focal adhesion kinase, are imperative for promotion of cell proliferation, survival and anti-apoptosis in cardiomyocytes by activation of their downstream pro-survival signalling molecules, such as the phosphorylated extracellular signal-regulated kinase1/2 (p-ERK1/2). As a component of the integrin pathway, C3G (Crk-SH3 domain guanine nucleotide exchange factor) protein may be involved in the promotion of cell proliferation and survival and anti-apoptosis in the H9C2 cardiomyocytes. Rat -derived H9C2 cardiomyocytes were transfected with pCXN2-flag-hC3G, a human C3G overexpression eukaryotic recombinant plasmid. Apoptosis, cell proliferation and survival were analysed in the H9C2 cardiomyocytes either treated with hypoxia/reoxygenation (H/R). Human C3G mRNA overexpression significantly elevated C3G protein expression in H9C2 cardiomyocytes whether treated with H/R or not. C3G overexpression promoted proliferation and survival and anti-apoptosis, and attenuated the proliferative and survival inhibition, and apoptosis induced by H/R by activation of its downstream pro-survival signalling molecule, p-ERK1/2. The results suggest that C3G acts as a pro-survival molecule in H9C2 cardiomyocytes by activation of p-ERK1/2.
- Subjects
INTEGRINS; HEART cells; CELL proliferation; NUCLEOTIDE exchange factors; KINASES
- Publication
Cell Biology International, 2013, Vol 37, Issue 10, p1106
- ISSN
1065-6995
- Publication type
Article
- DOI
10.1002/cbin.10136