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

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Biochemistry (Moscow) Supplement Series A: Membrane and Cell Biology Aims and scope

Abstract

Activation of phospholipase C (PLC)-linked signaling cascades in nonexcitable cells stimulates Ca2+ release from inositol-1,4,5-trisphosphate (IP3)-sensitive intracellular Ca2+ stores and activation of Ca2+ entry via plasma membrane Ca2+ channels. The attention of investigators is currently focused on the properties and molecular basis of channels involved in Ca2+ entry into nonexcitable cells. According to current views, mammalian TRP proteins are involved in receptor-and store-dependent influx of Ca2+; however, little is known about the linkage between specific TRP proteins and endogenous channels responsible for Ca2+ entry. The aim of the present study was to elucidate the role of TRPC3 in the formation of store-dependent or receptor-operated pathways of Ca2+ entry into A431 cells. Registration of Ca2+ influx based on fluorescence measurements of intracellular Ca2+ concentrations and analysis of integral membrane currents revealed that partial inhibition of TRPC3 expression by small interfering RNA (siRNA) results in suppression of store-dependent Ca2+ entry without any effect on receptor-operated Ca2+ influx. In-depth studies of single channels revealed that TRPC3 suppression in A431 cells results in the disappearance of one type of store-operated channels and formation of a novel type of store-independent Ca2+-permeable channels. This, in turn, testifies to the crucial role of TRPC3 in normal functioning of store-operated Ca2+ channels in A431 cells.

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Original Russian Text © E.V. Kaznacheyeva, L.N. Glushankova, V.V. Bugaj, O.A. Zimina, A.Yu. Skopin, V.A. Alexeenko, I.B. Bezprozvanny, and G.N. Mozhayeva, 2007, published in Biologicheskie Membrany, 2007, Vol. 24, No. 1, pp. 87–95.

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Kaznacheyeva, E.V., Glushankova, L.N., Bugaj, V.V. et al. Role of TRPC3 in the formation of receptor-and store-operated calcium channels in carcinoma A431 cells. Biochem. Moscow Suppl. Ser. A 1, 79–87 (2007). https://doi.org/10.1134/S1990747807010096

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  • DOI: https://doi.org/10.1134/S1990747807010096

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