Interference with endogenous ras function inhibits cellular responses to wounding.
Interference with endogenous ras function inhibits cellular responses to wounding.
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干扰内源性 ras 功能会抑制细胞对受伤的反应。
DOI：
10.1083/jcb.121.1.113
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发表时间：
1993
期刊：
影响因子：
--
通讯作者：
Feramisco,JR
中科院分区：
文献类型：
--
作者：
Sosnowski,RG;Feldman,S;Feramisco,JR
组织损伤会诱导细胞反应，最终导致伤口修复。在组织培养模型系统中的研究表明，这些反应包括AP-1调节基因的诱导、细胞迁移和有丝分裂，这些也是细胞对生长因子反应的特征。研究发现，细胞ras蛋白是生长因子刺激的信号转导通路的重要组成部分，但它们在创伤反应中的作用尚不清楚。利用静止的活体牛角膜内皮细胞(BCE)，显微注射ras显性干扰突变蛋白(N17)，然后用机械创伤刺激，研究c-ras在这一过程中的潜在参与。对这些细胞的分析表明，显微注射显性干扰ras蛋白，而不是对照蛋白，抑制了损伤反应，表现为Fos表达减少，细胞迁移不足，DNA合成受阻。
Wounding of tissue induces cellular responses that ultimately result in wound repair. Studies in tissue culture model systems indicate that these responses include induction of AP-1 regulated genes, cell migration and mitogenesis which are also characteristic of cellular responses to growth factors. Investigations have identified cellular ras proteins as critical components of growth factor-stimulated signal transduction pathways, however their role in the wounding response is less clear. Investigation of the potential involvement of c-Ras in this process utilized quiescent living bovine corneal endothelium cells (BCE) which were microinjected with ras dominant interfering mutant protein (N17) and subsequently stimulated by mechanical wounding. Analysis of these cells demonstrated that microinjection of dominant-interfering ras protein, but not control proteins, inhibited the wounding response as evidenced by diminished Fos expression, lack of cell migration and a block in DNA synthesis.