Role of the F-actin cytoskeleton in the RVD and RVI processes in Ehrlich ascites tumor cells
Role of the F-actin cytoskeleton in the RVD and RVI processes in Ehrlich ascites tumor cells
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DOI:
10.1006/excr.1999.4615
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发表时间:
1999-10-10
影响因子:
3.7
通讯作者:
Hoffmann, EK
中科院分区:
文献类型:
--
作者:
Pedersen, SF;Mills, JW;Hoffmann, EK
The role of the F-actin cytoskeleton in cell volume regulation was studied in Ehrlich ascites tumor cells, using a quantitative rhodamine-phalloidin assay, confocal laser scanning microscopy, and electronic cell sizing. A hypotonic challenge (180 mOsm) was associated with a decrease in cellular F-actin content at 1 and 3 min and a hypertonic challenge (600 mOsm) with an increase in cellular F-actin content at 1, 3, and 5 min, respectively, compared to isotonic (310 mOsm) control cells. Confocal visualization of F-actin in fixed, intact Ehrlich cells demonstrated that osmotic challenges mainly affect the F-actin in the cortical region of the cells, with no visible changes in F-actin in other cell regions. The possible role of the F-actin cytoskeleton in RVD was studied using 0.5 mu M cytochalasin B (CB), cytochalasin D (CD), or chaetoglobosin C (ChtC), a cytochalasin analog with little or no affinity for F-actin.Recovery of cell volume after hypotonic swelling was slower in cells pretreated for 3 min with 0.5 mu M CB, but not in CD- and ChtC-treated cells, compared to osmotically swollen control cells. Moreover, the maximal cell volume after swelling was decreased in CB-treated, but not in CD- or Chtc-treated cells. Following a hypertonic challenge imposed using the RVD/RVI protocol, recovery from cell shrinkage was slower in CB-treated, but not in CD- or Chtc-treated cells, whereas the minimal cell volume after shrinkage was unaltered by either of these treatments. It is concluded that osmotic cell swelling and shrinkage elicit a decrease and an increase in the F-actin content in Ehrlich cells, respectively. The RVD and RVI processes are inhibited by 0.5 mu M CB, but not by 0.5 mu M CD, which is more specific for actin. (C) 1999 Academic Press.