Effect of Apelin on Angiotensin II-induced Cardiomyocyte Hypertrophy With its Mechanism in Experimental Rats
10.3969/j.issn.1000-3614.2014.09.019
- VernacularTitle:Apelin对血管紧张素Ⅱ诱导的心肌细胞肥大的作用及其机制
- Author:
Ying ZHOU
;
Youzhou CHEN
;
Shubin QIAO
- Publication Type:Journal Article
- Keywords:
Angiotensin II;
Cardiomyocyte hypertrophy;
Calcineurin;
Calmodulin kinase II
- From:
Chinese Circulation Journal
2014;(9):733-737
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To explore the effect of apelin on angiotensin II (Ang II)-induced cardiomyocyte hypertrophy and intracellular signal transduction mechanism in experimental rats.
Methods: The cardiomyocyte from 1 to 3 days neonatal rats were cultured with Ang II to induce the cardiomyocyte hypertrophy, and the cells were treated by apelin at different concentrations. The [3H] Leucine incorporation, cardiomyocyte surface area and total protein expression were analyzed to evaluate the degree of cardiomycyte hypertrophy. The protein expressions of intracellular BNP, β-MHC, nuclear factor 3 of activated T cells (NFATc3), calcineurin, phospho-calcineurin, calmodulin kinase II (CaMK II) and phospho-CaMK II were assessed by Western blot analysis. The mRNA expressions of BNP andβ-MHC were examined by RT-PCR.
Results: Apelin may inhibit Ang II induced cardiomyocyte hypertrophic response in a dose-dependent manner, the maximum inhibition was achieved at Ang II 1000 nmol/L. Meanwhile, apelin may inhibit Ang II-induced elevations of intracellular resting free calcium level, mRNA expressions of BNP andβ-MHC, protein expressions of NFATc3, phospho-calcineurin, CaMK II and phospho-CaMK II in a dose-dependent manner.
Conclusion: Apelin may inhibit Ang II-induced cardiomyocyte hypertrophy in experimental rats which might be related to Ca2+-dependent calcineurin signal pass ways.
