Fibroblast quiescence in floating or released collagen matrices
Fibroblast quiescence in floating or released collagen matrices
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DOI：
10.1074/jbc.m101898200
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发表时间：
2001-08-17
影响因子：
4.8
通讯作者：
Grinnell, F
中科院分区：
文献类型：
--
作者：
Fringer, J;Grinnell, F
附着胶原基质中的成纤维细胞增殖，而漂浮或释放基质中的细胞变得静止。附着基质中的细胞具有突出的肌动蛋白应力纤维，表明它们处于等长张力下，而漂浮或释放基质中的成纤维细胞不存在应力纤维。与贴壁基质中的细胞相比，漂浮或释放基质中的细胞表现出细胞周期蛋白DI的下调和p27（Kip1）细胞周期蛋白依赖性激酶抑制剂的上调，并且贴壁基质中的细胞在被UO 126阻断ERK信号通路后也出现类似的变化。一个不同的模式发生在细胞周期调控蛋白的变化，但是，血清剥夺或肌动蛋白细胞骨架解聚的latrunculin B，这并没有阻止通过ERK途径的信号。因此，漂浮或释放胶原基质中的细胞静止可以通过ERK途径的信号传导减少来解释，但这些变化不能通过细胞中不存在等长张力来解释。
Fibroblasts in attached collagen matrices proliferate, whereas cells in floating or released matrices become quiescent. Cells in attached matrices had prominent actin stress fibers, indicating that they were under isometric tension, whereas stress fibers were absent from fibroblasts in floating or released matrices. Compared with cells in attached matrices, cells in floating or released matrices showed downregulation of cyclin DI and up-regulation of p27(Kip1) cyclin-dependent kinase inhibitor, and similar changes occurred after the ERK signaling pathway was blocked by UO126 in cells in attached matrices. A different pattern of changes in cell cycle regulatory proteins occurred, however, after serum deprivation or actin cytoskeletal depolymerization by latrunculin B, which did not prevent signaling through the ERK pathway. Therefore, cell quiescence in floating or released collagen matrices could be explained by decreased signaling through the ERK pathway, but these changes were not accounted for by the absence of isometric tension in the cells.