Unloading of intercellular tension induces the directional translocation of PKCα

Toshihiro Sera, Masataka Arai, Zhonghua Cui, Koichi Onose, Alireza Karimi, Susumu Kudo

Research output: Contribution to journalArticle

Abstract

The migration of endothelial cells (ECs) is closely associated with a Ca2+-dependent protein, protein kinase Cα (PKCα). The disruption of intercellular adhesion by single-cell wounding has been shown to induce the directional translocation of PKCα. We hypothesized that this translocation of PKCα is induced by mechanical stress, such as unloading of intercellular tension, or by intercellular communication, such as gap junction-mediated and paracrine signaling. In the current study, we found that the disruption of intercellular adhesion induced the directional translocation of PKCα even when gap junction-mediated and paracrine signaling were inhibited. Conversely, it did not occur when the mechanosensitive channel was inhibited. In addition, the strain field of substrate attributable to the disruption of intercellular adhesion tended to be larger at the areas corresponding with PKCα translocation. Recently, we found that a direct mechanical stimulus induced the accumulation of PKCα at the stimulus area, involving Ca 2+ influx from extracellular space. These results indicated that the unloading of intercellular tension induced directional translocation of PKCα, which required Ca 2+ influx from extracellular space. The results of this study indicate the involvement of PKCα in the Ca 2+ signaling pathway in response to mechanical stress in ECs.

Original languageEnglish
Pages (from-to)9764-9777
Number of pages14
JournalJournal of cellular physiology
Volume234
Issue number6
DOIs
Publication statusPublished - Jun 2019

All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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