质膜的损伤修复及相关模型

生物膜的磷脂双分子层将细胞与外界环境分开。大部分细胞会在机械损伤或化学应激下引发质膜损伤，如果不及时修复将会导致细胞死亡。胞外钙离子通过伤口进入细胞，作为损伤的最初信号，会诱发一系列的修复反应。随后，胞内细胞器也释放钙离子，并产生系列细胞行为来应对损伤，维护质膜的完整性。本文介绍了在损伤修复过程的胞吞作用、胞吐作用、胞外小泡脱落等细胞行为。综述了补丁模型、修复帽模型和大损伤修复的模型特点。补丁模型是最早的修复模型，提出后不断得到完善。细胞除了需要在损伤处聚集小泡、融合形成补丁外，还需通过胞吐、胞吞和出芽（小泡脱落）等方式参与伤口修复。本文简要介绍参与质膜修复的重要蛋白质如钙蛋白酶、dysferlin、MG53、膜联蛋白、突触结合蛋白(Syt-VⅡ)、ESCRTⅢ、酸性鞘磷脂酶、细胞骨架蛋白质等在修复过程中的作用。

Models in the Repair of Plasma Membrane Wounds

Eukaryotic cells from extracellular environments are separated by plasma membranes composed of phospholipid bilayers. Most cells are subject to mechanical or chemical stresses that could disrupt the plasma membrane. If these disruptions are not closed rapidly, it may lead to the cell deaths. As a result, cells have evolved active strategies to mend the broken membranes. A series of repair responses would be induced by extracellular calcium ions to enter cells through lesions as a primary signal. Then, intracellular calcium ions were released from intracellular organelles.A number of proteins were recruited to deal with the damage and maintain the integrity of the plasma membrane. This article introduces cell behaviors including the endocytosis, exocytosis, budding/blebbing, and reviewed the patch model, the repairing cap model, and the large wounds repairing. The patch model is the earliest repair model, and has been revised continuously. The wound repair process needs vesicles aggregation, vesicle fusion to form patches, and also via exocytosis, endocytosis and blebbing of extracellular vesicles. We will also introduce proteins related to membrane repair, including calpain, dysferlin, MG53, annexins, Syt-VII, ESCRT-III, acidic sphingomyelinase and cytoskeleton protein.