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通过类似于神经递质释放的囊泡机制进行细胞膜重封。

Cell membrane resealing by a vesicular mechanism similar to neurotransmitter release.

作者信息

Steinhardt R A, Bi G, Alderton J M

机构信息

Department of Molecular and Cell Biology, University of California, Berkeley 94720.

出版信息

Science. 1994 Jan 21;263(5145):390-3. doi: 10.1126/science.7904084.

Abstract

After injury to the cell membrane, rapid resealing of the membrane occurs with little loss of intracellular contents. This process has been studied by measurement of the rate of dye loss after membrane puncture in both the sea urchin embryo and 3T3 fibroblasts. Resealing of disrupted cell membranes requires external calcium that can be antagonized by magnesium. Block of multifunctional calcium/calmodulin kinase, which regulates exocytotic vesicle availability at synapses, and of kinesin, which is required for outward-directed transport of vesicles, inhibited membrane resealing. Resealing was also inhibited by botulinum neurotoxins B and A, suggesting that the two synaptosomal-associated proteins synaptobrevin and SNAP-25 also participate in resealing. This pattern of inhibition indicates that the calcium-dependent mechanisms for cell membrane resealing may involve vesicle delivery, docking, and fusion, similar to the exocytosis of neurotransmitters.

摘要

细胞膜受损后,细胞膜会迅速重新封闭,细胞内物质很少流失。通过测量海胆胚胎和3T3成纤维细胞膜穿刺后染料流失的速率,对这一过程进行了研究。破裂细胞膜的重新封闭需要外部钙,而镁可以拮抗这种钙。多功能钙/钙调蛋白激酶的阻断,该激酶调节突触处胞吐小泡的可用性,以及驱动蛋白的阻断,小泡向外运输需要驱动蛋白,均抑制了膜的重新封闭。肉毒杆菌神经毒素B和A也抑制了重新封闭,这表明两种突触体相关蛋白突触小泡蛋白和SNAP-25也参与了重新封闭。这种抑制模式表明,细胞膜重新封闭的钙依赖机制可能涉及小泡的递送、对接和融合,类似于神经递质的胞吐作用。

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