| Literature DB >> 28577190 |
Peiying Pai1,2, Bharath Kumar Velmurugan1,3, Chia-Hua Kuo1,4, Chung-Yi Yen1,2, Tsung-Jung Ho1,5,6, Yueh-Min Lin1,7,8, Yu-Feng Chen1,9, Chao-Hung Lai1,10, Cecilia Hsuan Day1,11, Chih-Yang Huang12,13,14,15.
Abstract
The present study was aimed to investigate the protective effects of 17β-estradiol (E2) and estrogen receptor α (ERα) on isoproterenol (ISO)-treated H9c2 cardiomyoblast cells. In the present study, we treated H9c2 cells with ISO, a β-adrenergic receptor agonist, to induce myocardiac hypertrophy. Pre-administration of E2 or ERα (induced by doxycycline) and E2 plus ERα significantly prevented ISO-induced increase of cell size and cytosolic calcium accumulation, accompanied with increased mRNA of atrial natriuretic peptide and brain natriuretic peptide. However, ICI-ERs antagonist, and melatonin, a specific inhibitor for ERα, reversed the cardioprotective effects, suggesting that E2 action was mediated through ERα. Further evidences showed that E2 and ERα increased the protein level of GSK3β and protein phosphatase 2a inhibitor 2 (I2-PP2A), which subsequently enhanced the activation of I2-PP2A by disrupting PP2A activity and maintains normal calcium outflow. Collectively, E2 and ERα inhibited hypertrophy by preventing cytosol calcium accumulation and by inhibiting the association between PP2A with Na+-Ca2+ exchanger via GSK3β and I2-PP2A activation.Entities:
Keywords: ANP; E2; Estrogen receptor alpha; GSK3β; H9c2 cells; ISO; PP2A
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Year: 2017 PMID： 28577190 DOI： 10.1007/s11010-017-3048-3
Source DB: PubMed Journal: Mol Cell Biochem ISSN： 0300-8177 Impact factor: 3.396