Both intact microtubules and actin filaments have been shown to be the primary interacting partners of lipid rafts. There is increasing evidence that lipid selleck catalog rafts in the cell mem brane are clustered in response to different stimuli to form signalling Inhibitors,Modulators,Libraries platforms for transmembrane transduction. Among these signalling platforms, Zhang et al. reported that some large redox signalling molecules are recruited into lipid raft microdomains and subsequently produce ROS in bovine coronary arterial endothelial cells. The present study comparing the binding of EGCg to EGFP expressing cells in conditions with or without H2O2 induced oxidative stress indicated that the strength of EGCg binding to cells exposed to H2O2 induced oxidative stress conditions doubled compared to controls without H2O2 exposure.

It appears that oxidative stress induced cardiac cells increase lipid raft signalling for the binding of EGCg. Accordingly, these rafts could function as platforms to mediate the EGCg intracellular signalling for cardioprotection against oxidative stress. Increasing evidence indicates that multiple signal transduction events in the heart Inhibitors,Modulators,Libraries occur via caveolae and caveolins to localize signalling molecules and recep tors in the membrane for cardioprotection. Both Cav 1 and Cav 3, functioning as scaffolding proteins, can provide direct temporal and spatial regulation with signalling molecules activated by a wide spectrum of Inhibitors,Modulators,Libraries cardioprotective agents including the volatile anesthetic isoflurane. Cav 1 has been shown to play a signalling role in cardiomyocytes.

In contrast, Cav 3, the muscle specific isoform, mediates interactions with cytoskel etal elements and is responsible for caveolae formation in cardiac cells. Several myocardial pathologies have been shown to be associated with alterations in Cav expression Cav 1 Inhibitors,Modulators,Libraries and Cav 3 levels are elevated in pressure overloaded and failing Inhibitors,Modulators,Libraries hearts, whereas reduced cardiac Cav 1 and Cav 3 expression has been reported in cases of myocardial infarction, cardiac hypertrophy, heart failure, and chronic hypoxia. Cav 1 levels are also altered in renal failure and pulmonary hyperten sion. In the present study, using in vitro H2O2 induced oxidative stress in H9c2 cells, we demonstrated that H2O2 caused a 30% decrease in the levels of Cav 1 concomitant with a 20% decrease in phosphorylated Cav 1, and these reductions were counteracted by 10 or 20 uM EGCg pre treatment for 30 min.

Since pre treatment with GSK 3B inhibitor, SB 216763, also blunted the effects of H2O2 induced oxidative stress on Cav 1 inhibition, it is very likely that EGCg could act through GSK 3B to affect selleck products Cav 1 signalling in H2O2 induced cells. The link between Cav 1 activation and GSK 3B signalling pathway could be achieved by Akt activation. Thus, during oxidative stress by myocardial ischemia assault Cavs can modulate intracellular signalling for EGCg medicated cardioprotection via Akt/GSK 3B path way.