Abstract
BackgroundEpigallocatechin-3-gallate (EGCg) with its potent anti-oxidative capabilities is known for its beneficial effects ameliorating oxidative injury to cardiac cells. Although studies have provided convincing evidence to support the cardioprotective effects of EGCg, it remains unclear whether EGCg affect trans-membrane signalling in cardiac cells. Here, we have demonstrated the potential mechanism for cardioprotection of EGCg against H2O2-induced oxidative stress in H9c2 cardiomyoblasts.ResultsExposing H9c2 cells to H2O2 suppressed cell viability and altered the expression of adherens and gap junction proteins with increased levels of intracellular reactive oxygen species and cytosolic Ca2+. These detrimental effects were attenuated by pre-treating cells with EGCg for 30 min. EGCg also attenuated H2O2-mediated cell cycle arrest at the G1-S phase through the glycogen synthase kinase-3β (GSK-3β)/β-catenin/cyclin D1 signalling pathway. To determine how EGCg targets H9c2 cells, enhanced green fluorescence protein (EGFP) was ectopically expressed in these cells. EGFP-emission fluorescence spectroscopy revealed that EGCg induced dose-dependent fluorescence changes in EGFP expressing cells, suggesting that EGCg signalling events might trigger proximity changes of EGFP expressed in these cells.Proteomics studies showed that EGFP formed complexes with the 67 kD laminin receptor, caveolin-1 and -3, β-actin, myosin 9, vimentin in EGFP expressing cells. Using in vitro oxidative stress and in vivo myocardial ischemia models, we also demonstrated the involvement of caveolin in EGCg-mediated cardioprotection. In addition, EGCg-mediated caveolin-1 activation was found to be modulated by Akt/GSK-3β signalling in H2O2-induced H9c2 cell injury.ConclusionsOur data suggest that caveolin serves as a membrane raft that may help mediate cardioprotective EGCg transmembrane signalling.
Highlights
Epigallocatechin-3-gallate (EGCg) with its potent anti-oxidative capabilities is known for its beneficial effects ameliorating oxidative injury to cardiac cells
EGCg cardioprotective effects on cell viability, reactive oxygen species (ROS) formation, and cytosolic Ca2+ overload in H2O2-treated H9c2 cells Previously, we have demonstrated that pre-treatment with green tea extract protects cardiomyocytes from regional myocardial ischemia by overcoming cytosolic Ca2+ overload, myofibril disruption, and alterations in adherens and gap junction protein levels and distribution in rats [4]
We used a cell model of H9c2 rat cardiomyoblast to verify the cardioprotection of EGCg against the H2O2-induced oxidative stress during myocardial ischemia assault
Summary
Epigallocatechin-3-gallate (EGCg) with its potent anti-oxidative capabilities is known for its beneficial effects ameliorating oxidative injury to cardiac cells. Studies have provided convincing evidence to support the cardioprotective effects of EGCg, it remains unclear whether EGCg affect trans-membrane signalling in cardiac cells. Studies have provided convincing evidence to support the cardioprotective effects of GTPs, it remains unclear whether GTPs affect trans-membrane signalling in cardiac cells. Another study with Cav-3 knockout mice subjected to IR injury has shown that the expression of Cav-3 in cardiac myocytes is essential for isoflurane-induced cardioprotection from myocardial ischemic injury [19]. These data suggested that Cav may mediate the beneficial actions of a variety of cardioprotective agents [19]
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