Exp Mol Med.  2009 Apr;41(4):226-235. 10.3858/emm.2009.41.4.025.

Modulation of the caveolin-3 localization to caveolae and STAT3 to mitochondria by catecholamine-induced cardiac hypertrophy in H9c2 cardiomyoblasts

Affiliations
  • 1Department of Biochemistry, Division of Applied Life Science (BK21), PMBBRC, Environmental Biotechnology National Core Research Center, Gyeongsang National University, Jinju, Korea. ybpak@nongae.gsnu.ac.kr

Abstract

We investigated the effect of phenylephrine (PE)- and isoproterenol (ISO)-induced cardiac hypertrophy on subcellular localization and expression of caveolin-3 and STAT3 in H9c2 cardiomyoblast cells. Caveolin-3 localization to plasma membrane was attenuated and localization of caveolin-3 to caveolae in the plasma membrane was 24.3% reduced by the catecholamine-induced hypertrophy. STAT3 and phospho-STAT3 were up-regulated but verapamil and cyclosporin A synergistically decreased the STAT3 and phospho-STAT3 levels in PE- and ISO-induced hypertrophic cells. Both expression and activation of STAT3 were increased in the nucleus by the hypertrophy. Immunofluorescence analysis revealed that the catecholamine-induced hypertrophy promoted nuclear localization of pY705-STAT3. Of interest, phosphorylation of pS727-STAT3 in mitochondria was significantly reduced by catecholamine-induced hypertrophy. In addition, mitochondrial complexes II and III were greatly down-regulated in the hypertrophic cells. Our data suggest that the alterations in nuclear and mitochondrial activation of STAT3 and caveolae localization of caveolin-3 are related to the development of the catecholamine-induced cardiac hypertrophy.

Keyword

cardiomegaly; caveolae; caveolin-3; cell nucleus; heart; isoproterenol; mitochondria; phenylephrine; STAT3 transcription factor

MeSH Terms

Animals
Catecholamines/*pharmacology
Caveolae/*metabolism
Caveolin 3/*metabolism
Cell Line
Hypertrophy/metabolism
Mitochondria/*metabolism
Myocardium/cytology/*pathology
Myocytes, Cardiac/cytology/*drug effects/metabolism
Rats
STAT3 Transcription Factor/*metabolism
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