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

DOI Web Site 34 References
  • Kevin Montagne
    Department of Mechanical Engineering, Graduate School of Engineering University of Tokyo Tokyo Japan
  • Takashi Ushida
    Department of Mechanical Engineering, Graduate School of Engineering University of Tokyo Tokyo Japan
  • Katsuko S. Furukawa
    Department of Bioengineering, Graduate School of Engineering University of Tokyo Tokyo Japan
  • Minki Chang
    Department of Bioengineering, Graduate School of Engineering University of Tokyo Tokyo Japan

Bibliographic Information

Published
2023-07-29
Resource Type
journal article
Rights Information
  • http://creativecommons.org/licenses/by-nc/4.0/
DOI
  • 10.1002/cbf.3834
Publisher
Wiley

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<jats:title>Abstract</jats:title><jats:p>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<jats:sup>2+</jats:sup> concentration. The differences between the increase in intracellular Ca<jats:sup>2+</jats:sup> concentration induced by cell poking and by ATP‐only stimulation have not been investigated. In this study, we investigated the Ca<jats:sup>2+</jats:sup> 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<jats:sup>2+</jats:sup> into the cytoplasm were not identical between cell poking and conventional ATP stimulation. The functions of the G protein‐coupled receptor (GPCR) subunits (Gq, G), ATP‐activated receptor and the upstream Ca<jats:sup>2+</jats:sup> release signal from the intracellular endoplasmic reticulum Ca<jats:sup>2+</jats:sup> store, were investigated. The results show that Gq plays a major role in the Ca<jats:sup>2+</jats:sup> response evoked by ATP‐only stimulation, while cell poking induces a Ca<jats:sup>2+</jats:sup> response requiring the involvement of both Gq and G units simultaneously. These results suggest that GPCR are not only activated by ATP‐only stimulation or autocrine ATP release during Ca<jats:sup>2+</jats:sup> signaling, but also activated by the mechanical effects of cell poking.</jats:p>

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