Intracellular calcium ion transients evoked by cell poking independently of released autocrine ATP in Madin-Darby canine kidney cells.

Abstract

The mechanical stimulation induced by poking cells with a glass needle activates Piezo1 receptors and the adenosine triphosphate (ATP) autocrine pathway, thus increasing intracellular Ca2+ concentration. The differences between the increase in intracellular Ca2+ concentration induced by cell poking and by ATP-only stimulation have not been investigated. In this study, we investigated the Ca2+ signaling mechanism induced by autocrine ATP release during Madin-Darby Canine Kidney cell membrane deformation by cell poking. The results suggest that the pathways for supplying Ca2+ into the cytoplasm were not identical between cell poking and conventional ATP stimulation. The functions of the G protein-coupled receptor (GPCR) subunits (G q, G ), ATP-activated receptor and the upstream Ca2+ release signal from the intracellular endoplasmic reticulum Ca2+ store, were investigated. The results show that G q plays a major role in the Ca2+ response evoked by ATP-only stimulation, while cell poking induces a Ca2+ response requiring the involvement of both G q and G units simultaneously. These results suggest that GPCR are not only activated by ATP-only stimulation or autocrine ATP release during Ca2+ signaling, but also activated by the mechanical effects of cell poking.