Gh partially mediates α1-adrenergic receptor-stimulated cardiac hypertrophy independent of Gq Regulation

Young Sup Byun, Woochul Chang, Soyeon Lim, Byeong Wook Song, Hye Jung Kim, Min Ji Cha, Yangsoo Jang, Namsik Chung, Ki Chul Hwang

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2 Citations (Scopus)


In cardiac myocytes, stimulation of α1-adrenoceptor(α1-AR) leads to hypertrophic phenomenon. The Gh protein is tissue type transglutaminase and transmits the intracellular signal with GTPase activity. Little is known about Gh-mediated intracellular signal transductions to develop the hypertrophy. The aim of this study was to elucidate how G h mediates norepinephrine(NE)-stimulated intracellular signal transductions leading to the hypertrophic responses in neonatal rat cardiomyocytes. NE-induced protein/DNA ratio and ERKs activation were inhibited by a α1-AR blocker(prazosin), but not by a β,-AR blocker(propranolol) . Gq mainly regulated protein/DNA ratio and genetic markers of hypertrophy but inhibition of Gq did not induce a decrease of hypertrophic response to the normal control. The treatment with siRNA for G h suppressed NE-induced PKC/MEK1, 2/ERKs activation. NE-induced β-MHC reorganization was inhibited by small interfering RNA targeting Gq or Gh. Cell surface area level of Gq inhibition was not the same as control but atrial natriuretic peptide(ANP), a cardiac hypertrophy marker, was inhibited by Gh and Gq suppression and coincidently inhibition of both Gh and Gq reduced the gene expression. These findings suggest that Gh is partially involved in the hypertrophic response induced by NE in cardiomyocytes through PKC/MEK1, 2/ERKs signal pathways via α1-AR/Gh.

Original languageEnglish
Pages (from-to)630-636
Number of pages7
JournalTissue Engineering and Regenerative Medicine
Issue number4-6
Publication statusPublished - 2008 Dec

All Science Journal Classification (ASJC) codes

  • Medicine (miscellaneous)
  • Biomedical Engineering


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