Modulation of the caveolin-3 localization to caveolae and STAT3 to mitochondria by catecholamine-induced cardiac hypertrophy in H9c2 cardiomyoblasts.
10.3858/emm.2009.41.4.025
- Author:
Kyuho JEONG
1
;
Hayeong KWON
;
Chanhee MIN
;
Yunbae PAK
Author Information
1. Department 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
- Publication Type:Original Article ; Research Support, Non-U.S. Gov't
- Keywords:
cardiomegaly;
caveolae;
caveolin-3;
cell nucleus;
heart;
isoproterenol;
mitochondria;
phenylephrine;
STAT3 transcription factor
- MeSH:
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
- From:Experimental & Molecular Medicine
2009;41(4):226-235
- CountryRepublic of Korea
- Language:English
-
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.
