After wounding, a G-protein coupled receptor promotes the restoration of tension in epithelial cells.

After wounding, a G-protein coupled receptor promotes the restoration of tension in epithelial cells.
复制标题

受伤后,G 蛋白偶联受体促进上皮细胞张力的恢复。

DOI:
10.1101/2023.05.31.543122
复制
发表时间:
2024
期刊:
bioRxiv : the preprint server for biology
影响因子:
--
通讯作者:
Hutson,MShane
Hutson,MShane
中科院分区:
--
文献类型:
--
作者:
Han,Ivy;Hua,Junmin;White,JamesS;O'Connor,JamesT;Nassar,LilaS;Tro,KadenJ;Page-McCaw,Andrea;Hutson,MShane

文献摘要

相似文献

上皮屏障功能的维持部分是由于细胞张力,细胞拉动它们的邻居以维持上皮的完整性。创伤中断细胞张力,并且创伤诱导的张力变化可作为启动上皮修复的早期信号。为了表征伤口如何改变细胞张力,我们使用了激光反冲试验来绘制果蝇蛹背的上皮单层伤口周围的皮质张力。在受伤后1分钟内,沿径向和切向方向沿着的皮质张力广泛丧失。这种张力损失与Rok失活时观察到的水平相似。张力随后恢复为向内的行波,在受伤后约10分钟到达伤口边缘。恢复张力需要GPCR MthllO和IP 3受体,这表明已知由细胞损伤激活的这种钙信号传导途径的重要性。张力恢复的波与先前报道的向内移动的收缩波相关;然而,收缩波本身不受MthllO敲低的影响。这些结果表明,细胞可以在没有MthllO信号传导的情况下瞬时增加张力和收缩,但是该途径对于在其被创伤破坏后完全重置基线上皮张力是至关重要的。
The maintenance of epithelial barrier function is due in part to cellular tension, with cells pulling on their neighbors to maintain epithelial integrity. Wounding interrupts cellular tension and wound-induced changes in tension may serve as an early signal to initiate epithelial repair. To characterize how wounds alter cellular tension, we used a laser-recoil assay to map cortical tension around wounds in the epithelial monolayer of the Drosophila pupal notum. Within a minute of wounding, there was widespread loss of cortical tension along both radial and tangential directions. This tension loss was similar to levels observed with Rok inactivation. Tension was subsequently restored as an inward traveling wave that reached the wound margin about 10 minutes after wounding. Restoring tension required the GPCR Mthl10 and the IP3 receptor, indicating the importance of this calcium signaling pathway known to be activated by cellular damage. The wave of tension restoration correlated with an inward-moving contractile wave that has been previously reported; however, the contractile wave itself was not affected by Mthl10 knockdown. These results indicate that cells may transiently increase tension and contract in the absence of Mthl10 signaling, but that pathway is critical for fully resetting baseline epithelial tension after it is disrupted by wounding.