Role of endothelin-1 and its receptors on hypertrophy or proliferation of cultured cardial cells.
- Author:
Hong-Wen YOU
1
;
Xi CHEN
;
Hong-Jie YOU
;
Yu-Qing ZHANG
;
Yan CAI
;
Guo-Zhang LIU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Animals, Newborn; Atrial Natriuretic Factor; biosynthesis; genetics; Cell Proliferation; Cells, Cultured; Endothelin-1; physiology; Fibroblasts; cytology; pathology; Hypertrophy; Myocytes, Cardiac; cytology; pathology; RNA, Messenger; biosynthesis; genetics; Rats; Rats, Sprague-Dawley; Receptor, Endothelin A; physiology
- From: Acta Academiae Medicinae Sinicae 2006;28(4):520-523
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the role of endothelin-1 and its receptors on hypertrophy or proliferation of cultured cardial cells.
METHODSCardiomyocytes and cardiac fibroblasts were isolated by trypsin digestion method, DNA and protein synthesis were measured by 3H-dexyribonucleotidethymine (3H-TdR) and 3H-Leucine (3H-Leu) incorporation, while protein content was measured by Bradford method. Atrial natriuretic peptide (ANP) mRNA expression of cardiomyocyte was measured by reverse transcripted-polymerase chain reaction. Selective endothelin (ET) receptor subtype antagonists BQ123 and BQ788 were used to block ET(A) receptors (ET(A)R) and ET(B)R respectively and to observe the effects of the two receptors during cardiac hypertrophy.
RESULTSET-1 significantly increased the 3H-TdR and 3H-Leu incorporation rate of cardiomyocytes and cardiac fibroblasts in a dose-dependent manner and increased protein content. Furthermore, ET-1 promoted the ANP mRNA expression of cardiomyocyte. ET(A)R antagonist remarkably blocked these effects, while ET(B)R antagonist had no obvious effect.
CONCLUSIONSET-1 can induce the hypertrophy for cardiomyocytes and the proliferation for cardiac fibroblasts. These effects are mediated by ET(A)R.
