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The expression of α-enolase in hypertrophic cardiomyocytes induced by endothelin-1(ET-1)and regulation mechanism for the expression / 中华老年医学杂志
Chinese Journal of Geriatrics ; (12): 851-855, 2008.
Article in Chinese | WPRIM | ID: wpr-397916
ABSTRACT
ObjectiveTo investigate the protein expression of ERK1/2,p-ERK1/2,HIF-1α and α-enolase in hypertrophic cardiomyocytes induced by ET-1 and explore the regulation mechanism of overexpression of α-enolase in hypertrophic cardiomyocytes.MethodsET-1-induced abnormal cardiomyocytes were used as model of cardiac hypertrophy.Cellsurface area, [<'3>H]-leucine incorporation and the actin staining were measured to determine the extent of hypertrophy. Cultured cardiomyocytes were divided into 4 groups at random, control group, PD98059 treated group, ET-1 treated group and PD980594- ET-1 treated group. The protein expressions of ERK1/2, p-ERK1/2,HIF-1α and α-enolase were detected by immunoblotting analysis.ResultsCompared with the control group , cell surface area and [<'3>H] leucine incorporation were increased in ET-1 treated group ((1350.7±107.5)μtm<'2> vs. (896.1±70. 2)μtm<'2> , P<0.05; (1387.9±14.8) dpm vs. (787.7±10.2)dpm,P<0.013. Actin staining showed that ET-1-treated cardiomyoeytes had more intense actin staining and clear cross-striations than did control group, which suggested that myocardial cell hypertrophy could be induced by ET-1 in WKY neonatal cardiomyocytes. After MEK 1/2 inhibitor PD98059 was used, the cell surface area and [<'3>H] leucine incorporation were decreased in PD980594-ET-1 treated group compared with ET-1 treated group[(907.0±92.5)μm<'2> vs. (1350.7±107.5)μm<'2>;(841.5±10. 5)dpm vs. (1387.9±14.8)dpm, both P<0.05], which suggested that myocardial cell hypertrophy could be regulated by ERK1/2 signal pathway. Immunoblotting analysis showed that the protein expressions of p-ERK1/2, HIF-1α and α-enolase increased after ET-1 treatment,while PD98059 as an inhibitor of the upstream kinase of ERK1/2 was used, the protein expressions of HIF-1α and α-enolase were partially inhibited.ConclusionsET-1 induces hypertrophic cardiomyocytes through ERK1/2 phosphorylation in cultured neonatal rat cardiac myocytes.ERK1/2 and HIF-1α signal pathway may play an important role in the overexpression of α-enolase in the hypertrophic cardiomyocytes.

Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Geriatrics Year: 2008 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Language: Chinese Journal: Chinese Journal of Geriatrics Year: 2008 Type: Article