模型细胞中的 p53 和钙调节的肌动蛋白重排。

The p53 and Calcium Regulated Actin Rearrangement in Model Cells.

机构信息

Medical School, Department of Biophysics, University of Pécs, H-7624 Pécs, Hungary.

Medical School, Institute of Physiology, University of Pécs, H-7624 Pécs, Hungary.

出版信息

Int J Mol Sci. 2022 Aug 13;23(16):9078. doi: 10.3390/ijms23169078.

DOI:10.3390/ijms23169078

PMID:36012344

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9408879/

Abstract

Long-term cellular stress maintains high intracellular Ca concentrations which ultimately initiates apoptosis. Our interest is focused on how the gelsolin (GSN) and junctional mediating and regulating Y protein (JMY) play important roles in stress response. Both of these proteins can bind p53 and actin. We investigated using in vitro fluorescence spectroscopy and found that the p53 competes with actin in GSN to inhibit p53-JMY complex formation. A high Ca level initializes p53 dimerization; the dimer competes with actin on JMY, which can lead to p53-JMY cotransport into the nucleus. Here we investigated how the motility and division rate of HeLa cells changes due to low-voltage electroporation of GSN or JMY in scratching assays. We revealed that JMY inhibits their motion, but that it can accelerate the cell division. GSN treatment slows down cell division but does not affect cell motility. HeLa cells fully recovered the gap 20 h after the electroporation with JMY and then started to release from the glass slides. Taken together, our in vitro results indicate that GSN and JMY may play an important role in the cellular stress response.

摘要

长期的细胞应激会保持细胞内钙离子浓度的升高，最终引发细胞凋亡。我们的研究兴趣集中在凝胶蛋白（GSN）和连接介导调节 Y 蛋白（JMY）如何在应激反应中发挥重要作用。这两种蛋白都可以与 p53 和肌动蛋白结合。我们通过体外荧光光谱法进行了研究，发现 p53 与肌动蛋白竞争与 GSN 结合，从而抑制 p53-JMY 复合物的形成。高钙水平会引发 p53 二聚化；二聚体与 JMY 上的肌动蛋白竞争，导致 p53-JMY 共转运进入细胞核。在这里，我们通过划痕实验研究了由于低电压电穿孔导致 GSN 或 JMY 转染后 HeLa 细胞的运动和分裂率如何变化。结果表明，JMY 抑制了细胞的运动，但可以加速细胞分裂。GSN 处理会减缓细胞分裂速度，但不会影响细胞运动。在 JMY 电穿孔后 20 小时，HeLa 细胞完全恢复了间隙，然后开始从载玻片上释放。综上所述，我们的体外结果表明，GSN 和 JMY 可能在细胞应激反应中发挥重要作用。