Gh Mediates α1-Adrenoceptor-Stimulated Hypertrophy Following
Ischemia/Reperfusion in Cardiomyocytes
Authors
Me Jin Kim ; Heesang Song ; Byeong-Wook Song ; Soyeon Lim ; Min-Ji Cha ; Eunju Choi ; Onju Ham ; Chang Yeon Lee ; Seong Yong Choi ; Se-Yeon Lee ; Ill Tae Hwang ; Yangsoo Jang ; Ki-Chul Hwang
Citation
TISSUE ENGINEERING AND REGENERATIVE MEDICINE, Vol.6(13) : 1282-1289, 2009
Ischemia/reperfusion (I/R) has been associated with ventricular (LV) remodeling, including induction of
hypertrophy. Stimulation of α1-Adrenoceptors (ARs) has been implicated in the pathogenesis of cardiac hypertrophy.
The present study is to test the hypothesis that α1-AR-mediated hypertrophy is selectively mediated via the oxidative
modification of Gh during hypoxia/reoxygenation (H/R) or I/R. Reactive oxygen species (ROS) was increased
in H/R and expression level of membrane Gh. To further address involvement of Gh in hypertrophic response, specific
relation of Gh was confirmed by using Gh overexpression and blocking into cardiomyocytes. Mainly increased
membrane Gh protein by ROS has a more sensitive effect on myocardial hypertrophy through MEK1,2/ERKs signal
transduction pathway, but induction of proto-oncogene except c-fos and expression of PLC δ1 was independent in
ROS condition. These results provide that ROS production by I/R mediates Gh protein increment and Gh protein
leads to more specific responsiveness to NE-stimulated hypertrophic cardiomyocytes