Effect of GA gene on di̇abeti̇c cardi̇ac hypertrophy and acti̇vati̇on of VEGFR2

It is known that G alfa11 knockout mice develop ventricular heart hypertrophy. But the role of vascular endothelial growth factor (VEGF) and activation of its receptor VEGFR2 in heart hypertrophy and in coronary angiogenesis remains to be clarified. To study the role of G alfa11 regulating phosphorylation of VEGFR2 in coronary blood vessels and in myocardial fibers of the diabetic animals, we induced diabetes mellitus (type 1) in wildtype and G alfa11 knockout mice. Expression of total VEGFR2 and localization of activated form of VEGFR2 were examined in coronary blood vessels and myocardial fibers by using quantitative immunohistochemistry. We detected a statisticaly significant decrease in expression total phosphorylated forms of VEGFR2. Same effect were found in myocardial fibers and coronary vessels. The staining intensities for p-VEGFR2 in G-protein G alfa11 Knockout Nondiabetic and G-protein G alfa11 Knockout Diabetic animals were weakly found than those of Wild-Type Nondiabetic and Wild-Type Diabetic animals. No difference was found in staining intensities of p-VEGFR2 in myocardial fibers between Wild-Type Nondiabetic and Wild-Type Diabetic animals. This finding indicates that G alfa11 is essential for the phosphorylation of VEGFR2 in myocardial fibers. Keywords: VEGF, VEGFR2, phosphorylation of VEGFR2, diabetes mellitus