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

Research output: Contribution to journalArticle

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.

Original languageEnglish
Pages (from-to)1282-1289
Number of pages8
JournalTissue Engineering and Regenerative Medicine
Volume6
Issue number13
Publication statusPublished - 2009 Oct 1

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Cardiac Myocytes
Adrenergic Receptors
Hypertrophy
Reperfusion
Reactive Oxygen Species
Ischemia
Oxygen
Proteins
Membranes
fos Genes
Signal transduction
Ventricular Remodeling
Cardiomegaly
Programmable logic controllers
Signal Transduction
Membrane Proteins
Hypoxia

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Biomedical Engineering

Cite this

Kim, M. J., Song, H., Song, B. W., Lim, S., Cha, M. J., Choi, E., ... Hwang, K. C. (2009). Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes. Tissue Engineering and Regenerative Medicine, 6(13), 1282-1289.
Kim, Me Jin ; Song, Heesang ; Song, Byeong Wook ; Lim, Soyeon ; Cha, Min Ji ; Choi, Eunju ; Ham, Onju ; Lee, Chang Yeon ; Choi, Seong Yong ; Lee, Se Yeon ; Hwang, Tae ; Jang, Yangsoo ; Hwang, Ki Chul. / Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes. In: Tissue Engineering and Regenerative Medicine. 2009 ; Vol. 6, No. 13. pp. 1282-1289.
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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.",
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Kim, MJ, Song, H, Song, BW, Lim, S, Cha, MJ, Choi, E, Ham, O, Lee, CY, Choi, SY, Lee, SY, Hwang, T, Jang, Y & Hwang, KC 2009, 'Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes', Tissue Engineering and Regenerative Medicine, vol. 6, no. 13, pp. 1282-1289.

Gh mediates α1-adrenoceptor-stimulated hypertrophy following ischemia/reperfusion in cardiomyocytes. / Kim, Me Jin; Song, Heesang; Song, Byeong Wook; Lim, Soyeon; Cha, Min Ji; Choi, Eunju; Ham, Onju; Lee, Chang Yeon; Choi, Seong Yong; Lee, Se Yeon; Hwang, Tae; Jang, Yangsoo; Hwang, Ki Chul.

In: Tissue Engineering and Regenerative Medicine, Vol. 6, No. 13, 01.10.2009, p. 1282-1289.

Research output: Contribution to journalArticle

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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 - 2009/10/1

Y1 - 2009/10/1

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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