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

The mechanical stimulation induced by poking cells with a glass needle activates Piezo1 receptors and the adenosine triphosphate (ATP) autocrine pathway, thus increasing intracellular Ca concentration. The differences between the increase in intracellular Ca concentration induced by cell poking and by ATP-only stimulation have not been investigated. In this study, we investigated the Ca 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 Ca 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 Ca release signal from the intracellular endoplasmic reticulum Ca store, were investigated. The results show that G q plays a major role in the Ca response evoked by ATP-only stimulation, while cell poking induces a Ca 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 Ca signaling, but also activated by the mechanical effects of cell poking.