Increased expression of Dock180 protein in the noninfarcted myocardium in rats

Abstract

The integrin β1 subunit and its downstream molecule focal adhesion kinase have been identified as critical molecules for the inhibition of postinfarction cardiac remodeling, ischemic cardiomyopathy, and heart failure. However, as a component of the integrin pathway, it is still unclear whether Dock180 (dedicator of cytokinesis 1) protein is expressed in the noninfarcted myocardium of the peri-infarct zones. In this study, experimental myocardial infarction (MI) and sham-operation (sham) models were established in Sprague Dawley rats and the expression of Dock180 protein in the myocardium of the sham group and in the noninfarcted myocardium of the peri-infarct zones of the MI group was detected by Western blot technique. The Dock180 protein expression in the myocardium was as follows: postsham 24-hour group, 0.10 ± 0.04 (n = 8); post-MI 24-hour group, 0.13 ± 0.03 (n = 8); postsham 12-week group, 0.11 ± 0.05 (n = 8); and post-MI 12-week group 0.17 ± 0.04 (n = 8). The Dock180 protein expression in the myocardium in the post-MI 12-week group was significantly higher than that in the postsham 12-week group (p = 0.019), in the postsham 24-hour group (p = 0.004), and in the post-MI 24-hour group (p = 0.040). We conclude that Dock180 protein is expressed in the myocardium in rats. Furthermore, its expression is significantly increased in the noninfarcted myocardium of the peri-infarct zones.

C3G overexpression promotes the survival of rat‐derived H9C2 cardiomyocytes by p‐ERK1/2

“…Apoptosis and survival inhibition in cardiomyocytes are among the major causes in the pathogenesis of many cardiovascular diseases such as diabetic and ischemic ventricular enlarged cardiomyopathy, systolic heart failure (Mu et al, 2011;Li et al, 2012a;Liu et al, 2013). A novel therapy targeting integrin pathway was developed for the patients with the cardiovascular diseases (Lal et al, 2007) due to its anti-apoptotic and pro-survival effects on the cardiomyocytes (Harston and Kuppuswamy, 2011;Figure 4 The apoptotic rate of H9C2 cardiomyocytes examined by flow cytometry.…”

Knockdown of CkrL by shRNA deteriorates hypoxia/reoxygenation‐induced H9C2 cardiomyocyte apoptosis and survival inhibition Via Bax and downregulation of P‐Erk1/2

“…[1][2][3] Increased apoptosis and cell survival inhibition in cardiomyocytes are the major causes of cardiomyocyte loss, ischemia/ reperfusion or H/R-induced myocardial injuries, postinfarction ventricular enlarged cardiomyopathy and systolic heart failure. 1,4,5 Targeting integrin pathway is a novel therapy measure for the previously mentioned cardiovascular diseases 6 because of its effects of cytoskeleton polymerisation and anti-apoptosis and prosurvival on the cardiomyocytes. 7,8 Integrin pathway links extracellular matrix substances to actin cytoskeleton in cardiomyocytes, and senses mechanical stretch, and translates it into intracellular biochemical signalling.…”