Role of TRPC3 in the formation of receptor- and store-operated calcium channels in A431 carcinoma cells

Activation of PLC-linked intracellular signaling cascades in the non-excitable cells evokes the release of calcium ions from the inositol 1,4,5-trisphosphate (InsP3)-sensitive intracellular Ca2+ stores and Ca2+ entry in the cytosol via Ca2+-channels of plasma membrane. The properties and molecular identity of these channels are now under intense investigation. It is speculated that mammalian proteins belonging to the TRP-related family take part in either receptor- and store- dependent entry, though data linking the specific TRP proteins and any endogenous Ca 2+- channel are very scarce. Thus we aimed to study the role of TRPC3 in the formation of receptor- and store- operated calcium entry pathways in A431 cells. Both whole-cell current recordings and fluorescent measurements of intracellular Ca2+ concentration have shown that partial inhibition of TRPC3 expression with small interfering RNAs (siRNA) suppresses the store-dependent Ca2+ entry, but does not affect the receptor-mediated Ca2+ entry. The investigations on the single-channel level revealed that TRPC3 suppression leads to the disappearance of one of the types of store operated Ca2+- channels in the plasma membrane and appearance of a new type of a store-independent channel in it. It might indicate that TRPC3 protein is needed for the functioning of store-dependent channel in A431 cells