Lyass L A, Bershadsky A D, Vasiliev J M, Gelfand I M
Laboratory of Molecular Biology and Bioorganic Chemistry, Moscow State University, U.S.S.R.
Proc Natl Acad Sci U S A. 1988 Dec;85(24):9538-41. doi: 10.1073/pnas.85.24.9538.
The effect of the tumor promoter phorbol 12-myristate 13-acetate (PMA) upon the contractility of permeabilized cell models (cytoskeletons) of mouse fibroblasts was examined. Contraction was induced by incubation of cell models in a solution containing ATP and was assessed quantitatively by measuring alterations of the area of cell model projection on the substrate. Immunofluorescence microscopy was used to assess alterations of cytoskeleton morphology in the course of permeabilization and contraction. It was found that contractility of cell models from PMA-treated fibroblasts was considerably diminished as compared with the models from control fibroblasts. ATP induced only local contraction of certain zones of actin cortex in models from PMA-treated fibroblasts; it did not induce general contraction, characteristic of control models. Normal high contractility was characteristic of the models from the cells preincubated with PMA in combination with Colcemid. PMA is a specific activator of protein kinase C, one of the key enzymes of the membrane signal-transduction pathway. It is suggested that protein kinase C regulates contractility of actin cortex and that the pathway of this regulation has a microtubule-dependent stage blocked by Colcemid.
研究了肿瘤启动子佛波醇12 -肉豆蔻酸酯13 -乙酸酯（PMA）对小鼠成纤维细胞透化细胞模型（细胞骨架）收缩性的影响。通过将细胞模型在含有ATP的溶液中孵育来诱导收缩，并通过测量细胞模型在底物上投影面积的变化进行定量评估。免疫荧光显微镜用于评估透化和收缩过程中细胞骨架形态的变化。结果发现，与对照成纤维细胞的模型相比，PMA处理的成纤维细胞的细胞模型的收缩性显著降低。ATP仅诱导PMA处理的成纤维细胞模型中肌动蛋白皮质某些区域的局部收缩；它不会诱导对照模型特有的整体收缩。与秋水仙酰胺联合预孵育PMA的细胞的模型具有正常的高收缩性。PMA是膜信号转导途径的关键酶之一蛋白激酶C的特异性激活剂。有人提出蛋白激酶C调节肌动蛋白皮质的收缩性，并且这种调节途径有一个被秋水仙酰胺阻断的微管依赖性阶段。
