Nitric oxide inhibits the expression of proto-oncogene c-fos induced by angiotensin Ⅱ and endothelin-1 in cardiomyocytes
10.3321/j.issn:0371-0874.2000.06.002
- VernacularTitle:一氧化氮抑制血管紧张素Ⅱ和内皮素-1诱导的心肌细胞原癌基因c-fos表达
- Author:
Chang-De ZHAN
1
;
Jing-Yun PAN
Author Information
1. 中山大学
- Keywords:
nitric oxide;
angiotensin Ⅱ;
endothelin-1;
c-fos;
protein kinase C
- From:
Acta Physiologica Sinica
2000;52(6):450-454
- CountryChina
- Language:Chinese
-
Abstract:
The effect of nitric oxide (NO) on the hypertrophic response and the proto-oncogene c-fos expression induced by angiotensin Ⅱ (AⅡ) or endothelin-1 (ET-1) was investigated in the primary culture of neonatal rat cardiomyocytes. Total protein content of cardiomyocytes (used as the index of cardiac myocyte hypertrophy) was determined by the Bradford method. The proto-oncogene c-fos expression was assessed using reverse transcription-polymerase chain reaction (RT-PCR) standardized with glyceraldehyde-3-phosphate dehydrogenase (GAPDH). RT-PCR was performed in a single tube using gene-specific primers and the SuperScript One-Step RT-PCR System. Total protein content of cardiomyocytes increased significantly on day 5 after AⅡ treatment or on day 3 after ET-1 treatment and the increased protein content was inhibited by SNP (NO donor). AⅡ, ET-1 and PMA (protein kinase C activator) induced the c-fos gene expression of cardiomyocytes, while L-arginine inhibited it. The L-arginine effect was blocked by L-NAME (NOS inhibitor). SNP inhibited the c-fos gene expression of cardiomyocytes induced by AⅡ,ET-1 or PMA as well. These results suggest that NO can inhibit the hypertrophic response and the proto-oncogene c-fos expression of cardiomyocytes induced by AⅡ or ET-1 and the cross-link may be located at the site of protein kinase C.
