Unloading of intercellular tension induces the directional translocation of PKCα
Unloading of intercellular tension induces the directional translocation of PKCα
复制标题
细胞间张力卸载诱导 PKCα 定向易位
DOI：
10.1002/jcp.27662
复制
发表时间：
2019
影响因子：
5.6
通讯作者：
Susumu Kudo,
中科院分区：
文献类型：
--
作者：
Toshihiro Sera;Masataka Arai;Zhunghua Cui;Koichi Onose;Alireza Karimi;Susumu Kudo,
内皮细胞（EC）的迁移与一种钙依赖性蛋白--蛋白激酶Cα（PKCα）密切相关。单细胞损伤导致的细胞间粘附的破坏已被证明可诱导PKCα的定向易位。我们假设PKCα的这种易位是由机械应力诱导的，如细胞间张力的卸载，或由细胞间通讯诱导的，如间隙连接介导的和旁分泌信号。在目前的研究中，我们发现，即使间隙连接介导的和旁分泌信号被抑制，细胞间粘附的破坏也会诱导PKCα的定向易位。相反，当机械敏感通道被抑制时，它不会发生。在PKCα转位对应的区域，细胞间粘附破坏所引起的底物应变场有较大的趋势。最近，我们发现直接的机械刺激可诱导PKCα在刺激区的积聚，涉及细胞外间隙的Ca 2+内流。这些结果表明，细胞间张力的释放导致PKCα定向移位，这需要细胞外Ca ~（2+）内流。本研究结果提示PKCα参与了内皮细胞对机械应力反应的Ca ~（2+）信号通路。
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 Ca2+influx from extracellular space. These results indicated that the unloading of intercellular tension induced directional translocation of PKCα, which required Ca2+influx from extracellular space. The results of this study indicate the involvement of PKCα in the Ca2+signaling pathway in response to mechanical stress in ECs.
登录
查看更多内容
通过 PKCα 的特异性抑制剂调节皮肤微血管血管生成、细胞迁移和渗透性。
影响因子：
6.5
作者：
S. Bokhari;Lisa Zhou;M. Karasek;Sarita G Paturi;V. Chaudhuri
通讯作者：
V. Chaudhuri
蛋白激酶 Cα 靶向受细胞内游离钙浓度 [Ca2+]i 的时间和空间变化调节
DOI：
10.1096/fj.99-0403com
发表时间：
2000
期刊：
The FASEB Journal
影响因子：
--
作者：
C. Maasch;S. Wagner;C. Lindschau;G. Alexander;K. Buchner;M. Gollasch;F. Luft;H. Haller
通讯作者：
H. Haller
影响因子：
3.3
作者：
Cherian, PP;Siller-Jackson, AJ;Jiang, JX
通讯作者：
Jiang, JX
DOI：
10.1016/s0021-9258(17)42143-0
发表时间：
1994-01
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Z. Szallasi;Colin B. Smith;G. Pettit;P. Blumberg
通讯作者：
Z. Szallasi;Colin B. Smith;G. Pettit;P. Blumberg
钙、二酰甘油和磷酸化在 PKCα-GFP* 时空调节中的相互作用
DOI：
10.1074/jbc.m201130200
发表时间：
2002
期刊：
The Journal of Biological Chemistry
影响因子：
--
作者：
A. Tanimura;A. Nezu;T. Morita;N. Hashimoto;Y. Tojyo
通讯作者：
Y. Tojyo