Abstract
The present study was performed to examine the effect of H2O2 on TRPC6 channel in HEK293t cells. In the TRPC6 expressing cells, H2O2 significantly stimulated Ca2+ entry in a dose‐dependent manner. This effect appeared through a distinct mechanism from DAG because the Ca2+ entry response and TRPC6 channel activity induced by a combination of OAG and H2O2 was significantly greater than the individual response of either OAG or H2O2. Inhibition of endogenous H2O2 by catalase substantially attenuated the OAG‐induced Ca2+ entry. NEM, a thiol‐specific oxidizing agent, were able to mimic the H2O2 response, and DTT, a thiol‐specific reducing agent, significantly inhibited the H2O2 response. DTNB, a cell membrane‐impermeable thiol oxidizing agent, did not affect TRPC6 channel activity when applied via the pipette solution in cell‐attached patches. Furthermore, the NEM‐induced TRPC6 activation was only observed in cell‐attached patches, but not in inside‐out patches. Taken together, these data indicate that H2O2 is an activator of TRPC6 channel. This H2O2 dependent response is through modification of thiol groups on intracellular proteins. Funding was provided by the American Diabetes Association.
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