Mills J W, Schwiebert E M, Stanton B A
Biology Department, Clarkson University, Potsdam, New York 12983.
J Exp Zool. 1994 Feb 1;268(2):111-20. doi: 10.1002/jez.1402680207.
Actin filaments could play a role in regulation of cell swelling by two distinct mechanisms. One is by a tensile mechanism involving the coordinated interaction of actin and actin-associated proteins with all plasma membrane domains. The actin-membrane linkage would restrain cell swelling in the event of the influx of water. In shark rectal gland cells, conditions that cause massive cell swelling (i.e., high K medium, exposure to mercurials) are associated with disruption of membrane-associated actin filaments. Under conditions that result in only moderate swelling (Na-pump inhibition, Li substitution) the actin filaments remain associated with the cell membrane. Thus, in this cell type, disruption of the actin-membrane organization is correlated with increased swelling. Another mechanism by which actin could limit cell swelling is via regulation of ion transport proteins that are activated by cell swelling. This could be accomplished by a vesicle transport and insertion mechanism that delivers ion transport units to the cell membrane or by interaction with transport proteins already present in the membrane. Cell-attached patch clamp studies of RCCT-28A cells exposed to hypotonic medium demonstrated the activation of Cl-channel activity coincident with an alteration in actin. Activation of the channel was mimicked by stretching the membrane. Exposure of inside-out patches to cytochalasins also increased Cl-channel activity. Treatment of isolated patches with phalloidin inhibited stretch-induced activation. Thus, regulation of a volume-sensitive Cl-channel appears to be directly related to the state of organization of actin filaments.
肌动蛋白丝可能通过两种不同机制在细胞肿胀调节中发挥作用。一种是通过拉伸机制,涉及肌动蛋白和肌动蛋白相关蛋白与所有质膜结构域的协同相互作用。在水流入的情况下,肌动蛋白 - 膜连接会抑制细胞肿胀。在鲨鱼直肠腺细胞中,导致大量细胞肿胀的条件(即高钾培养基、接触汞剂)与膜相关肌动蛋白丝的破坏有关。在仅导致适度肿胀的条件下(钠泵抑制、锂替代),肌动蛋白丝仍与细胞膜相关。因此,在这种细胞类型中,肌动蛋白 - 膜组织的破坏与肿胀增加相关。肌动蛋白限制细胞肿胀的另一种机制是通过调节因细胞肿胀而被激活的离子转运蛋白。这可以通过将离子转运单元递送至细胞膜的囊泡运输和插入机制来实现,或者通过与膜中已存在的转运蛋白相互作用来实现。对暴露于低渗培养基的RCCT - 28A细胞进行的细胞贴附式膜片钳研究表明,Cl通道活性的激活与肌动蛋白的改变同时发生。通过拉伸膜可模拟通道的激活。将外翻膜片暴露于细胞松弛素也会增加Cl通道活性。用鬼笔环肽处理分离的膜片可抑制拉伸诱导的激活。因此,对容积敏感的Cl通道的调节似乎与肌动蛋白丝的组织状态直接相关。