Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes

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; Tae Hwang; Yangsoo Jang; Ki Chul Hwang

G_h mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes

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, Tae Hwang, Yangsoo Jang, Ki Chul Hwang

Department of Internal Medicine

Research output: Contribution to journal › Article › peer-review

Abstract

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 G_h during hypoxia/reoxygenation (H/R) or I/R. Reactive oxygen species (ROS) was increased in H/R and expression level of membrane G_h. To further address involvement of G_h in hypertrophic response, specific relation of G_h was confirmed by using G_h overexpression and blocking into cardiomyocytes. Mainly increased membrane G_h 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 G _h protein increment and G_h protein leads to more specific responsiveness to NE-stimulated hypertrophic cardiomyocytes.

Original language	English
Pages (from-to)	1282-1289
Number of pages	8
Journal	Tissue Engineering and Regenerative Medicine
Volume	6
Issue number	13
Publication status	Published - 2009 Oct

All Science Journal Classification (ASJC) codes

Medicine (miscellaneous)
Biomedical Engineering

Cite this

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title = "Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes",

abstract = "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 G h protein increment and Gh protein leads to more specific responsiveness to NE-stimulated hypertrophic cardiomyocytes.",

author = "Kim, {Me Jin} and Heesang Song and Song, {Byeong Wook} and Soyeon Lim and Cha, {Min Ji} and Eunju Choi and Onju Ham and Lee, {Chang Yeon} and Choi, {Seong Yong} and Lee, {Se Yeon} and Tae Hwang and Yangsoo Jang and Hwang, {Ki Chul}",

year = "2009",

month = oct,

language = "English",

volume = "6",

pages = "1282--1289",

journal = "Tissue Engineering and Regenerative Medicine",

issn = "1738-2696",

publisher = "Springer Science + Business Media",

number = "13",

}

TY - JOUR

T1 - Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes

AU - Kim, Me Jin

AU - Song, Heesang

AU - Song, Byeong Wook

AU - Lim, Soyeon

AU - Cha, Min Ji

AU - Choi, Eunju

AU - Ham, Onju

AU - Lee, Chang Yeon

AU - Choi, Seong Yong

AU - Lee, Se Yeon

AU - Hwang, Tae

AU - Jang, Yangsoo

AU - Hwang, Ki Chul

PY - 2009/10

Y1 - 2009/10

N2 - 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 G h protein increment and Gh protein leads to more specific responsiveness to NE-stimulated hypertrophic cardiomyocytes.

AB - 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 G h protein increment and Gh protein leads to more specific responsiveness to NE-stimulated hypertrophic cardiomyocytes.

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M3 - Article

AN - SCOPUS:84884557939

SN - 1738-2696

VL - 6

SP - 1282

EP - 1289

JO - Tissue Engineering and Regenerative Medicine

JF - Tissue Engineering and Regenerative Medicine

IS - 13

ER -

G_h mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes

Abstract

All Science Journal Classification (ASJC) codes

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