Department of Anatomy, St. Marianna University School of Medicine, 2-16-1 Sugao, Miyamae, Kawasaki, Kanagawa 216-8511, Japan.
Biochem Biophys Res Commun. 2019 Mar 26;511(1):161-164. doi: 10.1016/j.bbrc.2019.02.061. Epub 2019 Feb 15.
Disruption and repair of plasma membranes is normally observed in many animal tissues. Recent studies demonstrated that wounding of Madin-Darby canine kidney cells potentiates membrane repair in cells adjacent to wounded cells via paracrine purinergic signaling. The present study demonstrated that cyclic adenosine monophosphate signaling in a wounded cell was induced by autocrine purinergic signaling, and protein kinase A potentiates membrane resealing for repeated wounds in those cells. Furthermore, the present study revealed that an increase in the intracellular free Ca concentration upon cell membrane disruption was not only due to Ca influx through the wound site, but also because of autocrine purinergic signaling. Although the influx of extracellular Ca is essential for membrane resealing, the present study suggested that an increase in the intracellular free Ca concentration induced by autocrine signaling accelerates membrane resealing of the initial cell membrane disruption.
在许多动物组织中，通常可以观察到质膜的破坏和修复。最近的研究表明，马兜铃酸肾病细胞的损伤通过旁分泌嘌呤能信号增强了邻近受伤细胞的膜修复。本研究表明，自分泌嘌呤能信号诱导受伤细胞中环磷酸腺苷单磷酸信号的产生，蛋白激酶 A 增强了这些细胞中重复损伤的膜封闭。此外，本研究揭示了质膜破坏时细胞内游离 Ca 浓度的增加不仅是由于通过伤口部位的 Ca 内流，还因为自分泌嘌呤能信号。虽然细胞外 Ca 的流入对于膜封闭是必需的，但本研究表明，自分泌信号诱导的细胞内游离 Ca 浓度的增加加速了初始质膜破坏的膜封闭。
