Role of liver X receptors on cardiomyocyte hypertrophy.
- Author:
Ran YIN
1
;
Meng-hong WANG
;
Yun-feng WEI
;
Yu-quan LI
;
Yu-gang DONG
Author Information
- Publication Type:Journal Article
- MeSH: Angiotensin II; pharmacology; Animals; Animals, Wild; Cells, Cultured; Hydrocarbons, Fluorinated; pharmacology; Liver X Receptors; Male; Mice; Mice, Inbred C57BL; Myocytes, Cardiac; drug effects; pathology; Orphan Nuclear Receptors; agonists; metabolism; Sulfonamides; pharmacology
- From: Chinese Journal of Cardiology 2009;37(12):1119-1123
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the expression of liver X receptors (LXR) in hypertrophic myocardium and the effect of LXR agonist T0901317 on angiotensin II (AngII) induced cardiomyocyte hypertrophy.
METHODSTransverse aortic coarctation (TAC) or sham operation were performed in 2-month-old wide type mice (C57/B6). Two weeks later, the expression of LXR in myocardium was detected by quantitative real-time PCR analysis and Western blot analysis. The effect of LXR agonist T0901317 on AngII-induced hypertrophy in cultured neonatal rat cardiomyocytes was also assessed.
RESULTSQuantitative real-time PCR analysis and Western blot analysis showed that LXRalpha but not LXRbeta expression was upregulated post TAC both at mRNA and protein levels (All P < 0.05). AngII induced increased [(3)H] leucine incorporation and cardiomyocyte hypertrophy were significantly reduced by T0901317 in a dose-dependent manner (P < 0.05). T0901317 also dose-dependently inhibited atrial natriuretic peptide (ANP) gene expression in cardiomyocytes (P < 0.05).
CONCLUSIONOur findings strongly suggest that LXR is a potent mediator of cardiomyocyte hypertrophy and LXR activation could attenuate AngII induced cardiomyocyte hypertrophy in vitro.