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 language | English |
|---|---|
| Pages (from-to) | 9764-9777 |
| Number of pages | 14 |
| Journal | Journal of cellular physiology |
| Volume | 234 |
| Issue number | 6 |
| DOIs | |
| Publication status | Published - Jun 1 2019 |
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All Science Journal Classification (ASJC) codes
- Physiology
- Clinical Biochemistry
- Cell Biology
Cite this
Unloading of intercellular tension induces the directional translocation of PKCα. / Sera, Toshihiro; Arai, Masataka; Cui, Zhonghua; Onose, Koichi; Karimi, Alireza; Kudo, Susumu.
In: Journal of cellular physiology, Vol. 234, No. 6, 01.06.2019, p. 9764-9777.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Unloading of intercellular tension induces the directional translocation of PKCα
AU - Sera, Toshihiro
AU - Arai, Masataka
AU - Cui, Zhonghua
AU - Onose, Koichi
AU - Karimi, Alireza
AU - Kudo, Susumu
PY - 2019/6/1
Y1 - 2019/6/1
N2 - 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.
AB - 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.
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UR - http://www.scopus.com/inward/citedby.url?scp=85055920598&partnerID=8YFLogxK
U2 - 10.1002/jcp.27662
DO - 10.1002/jcp.27662
M3 - Article
C2 - 30387146
AN - SCOPUS:85055920598
VL - 234
SP - 9764
EP - 9777
JO - Journal of Cellular Physiology
JF - Journal of Cellular Physiology
SN - 0021-9541
IS - 6
ER -