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.
journal_name
Mol Cell Biochemjournal_title
Molecular and cellular biochemistryauthors
Pai P,Velmurugan BK,Kuo CH,Yen CY,Ho TJ,Lin YM,Chen YF,Lai CH,Day CH,Huang CYdoi
10.1007/s11010-017-3048-3subject
Has Abstractpub_date
2017-10-01 00:00:00pages
181-195issue
1-2eissn
0300-8177issn
1573-4919pii
10.1007/s11010-017-3048-3journal_volume
434pub_type
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