Plasma membrane damage sensing and repairing. Role of heterotrimeric G-proteins and the cytoskeleton
Plasma membrane damage sensing and repairing. Role of heterotrimeric G-proteins and the cytoskeleton
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DOI：
10.1016/j.tiv.2011.04.009
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发表时间：
2011-08-01
影响因子：
3.2
通讯作者：
Panaro, Maria Antonietta
中科院分区：
文献类型：
--
作者：
Calvello, Rosa;Mitolo, Vincenzo;Panaro, Maria Antonietta
来自细菌、病毒或免疫系统细胞的不同毒剂以及细胞运动过程中产生的机械力能够打开细胞质膜中的孔。这些生物制剂中的大多数通过特定受体起作用。我们研究了温和的非离子去污剂Triton X-100产生的“非特异性”质膜孔的形成和重新密封。在HL-60衍生的粒细胞质膜孔开放后，1小时的Triton X-100处理的记录进入细胞的膜不渗透染料溴化乙锭。作为孔开放的结果，细胞内K+浓度福尔斯显著下降，细胞溶质pH降低，细胞膜去极化。此外，细胞获得极化形态，证明肌动蛋白细胞骨架的参与。在Triton浓度下，膜损伤逐渐修复，到8小时，对溴化乙锭的不渗透性恢复，细胞内K+浓度几乎正常。在用Triton +百日咳毒素、Triton +细胞松弛素或Triton +百日咳毒素+细胞松弛素处理后，膜修复的进程显著减慢，并且在8小时时不再完成。它的结论是，膜损伤激活百日咳敏感的G-蛋白可能作为传感器的损害，而G-蛋白和肌动蛋白细胞骨架参与膜修复机制。(C)2011爱思唯尔有限公司保留所有权利。
Different toxic agents, derived from bacteria, viruses or cells of the immune system, as well as mechanical forces generated during cell locomotion are able to open pores in the cell plasma membrane. Most of these biological agents operate through specific receptors. We studied the formation and resealing of the "non-specific" plasma membrane pores generated by the mild non-ionic detergent Triton X-100. In HL-60-derived granulocytic cells plasma membrane pore opening after a 1-h treatment with Triton X-100 is documented by entry into the cell of the membrane impermeant dye ethidium bromide. As a consequence of the opening of pores the intracellular K+ concentration falls dramatically, the cytosolic pH diminishes and the cell membrane is depolarized. Furthermore the cells acquire a polarized morphology, demonstrating the involvement of the actin cytoskeleton. At the Triton concentration used the membrane lesions are progressively repaired and by 8 h the impermeability to ethidium bromide is restored and the intracellular K+ concentration is virtually normal. Following treatments with Triton + Pertussis toxin, Triton + Cytochalasin, or Triton + Pertussis toxin + Cytochalasin the progress of membrane repair is dramatically slowed and is no longer completed by 8 h. It is concluded that the membrane damage activates pertussis-sensitive G-proteins which likely act as sensors of the damage, while both G-proteins and the actin cytoskeleton are involved in the membrane repair mechanism. (C) 2011 Elsevier Ltd. All rights reserved.