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首页> 外文期刊>Journal of Cellular Physiology >PED/PEA-15 controls fibroblast motility and wound closure by ERK1/2-dependent mechanisms
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PED/PEA-15 controls fibroblast motility and wound closure by ERK1/2-dependent mechanisms

机译：PED / PEA-15控制纤维母细胞的能动性和伤口关闭通过ERK1/2-dependent机制

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摘要

Cell migration is dependent on the control of signaling events that play significant roles in creating contractile force and in contributing to wound closure. We evaluated wound closure in fibroblasts from mice overexpressing (TgPED) or lacking ped/pea-15 (KO), a gene overexpressed in patients with type 2 diabetes. Cultured skin fibroblasts isolated from TgPED mice showed a significant reduction in the ability to recolonize wounded area during scratch assay, compared to control fibroblasts. This difference was observed both in the absence and in the presence of mytomicin C, an inhibitor of mitosis. In time-lapse experiments, TgPED fibroblasts displayed about twofold lower velocity and diffusion coefficient, as compared to controls. These changes were accompanied by reduced spreading and decreased formation of stress fibers and focal adhesion plaques. At the molecular level, TgPED fibroblasts displayed decreased RhoA activation and increased abundance of phosphorylated extracellular signal-regulated kinase 1/2 (ERK1/2). Inhibition of ERK1/2 activity by PD98059 restored RhoA activation, cytoskeleton organization and cell motility, and almost completely rescued wound closure of TgPED fibroblasts. Interestingly, skin fibroblasts isolated from KO mice displayed an increased wound closure ability. In vivo, healing of dorsal wounds was delayed in TgPED and accelerated in KO mice. Thus, PED/PEA-15 may affect fibroblast motility by a mechanism, at least in part, mediated by ERK1/2. J. Cell.
机译：细胞迁移是依赖的控制信号事件中扮演重要的角色创建收缩力和贡献伤口关闭。成纤维细胞从老鼠overexpressing(记者)或缺乏ped / pea-15 (KO),基因过表达2型糖尿病患者。成纤维细胞与三峡工程老鼠了显著减少的能力开拓殖民地受伤区域划痕试验期间,而控制成纤维细胞。都被观察到在没有在吗mytomicin C,有丝分裂抑制剂。在延时实验中,三峡工程的成纤维细胞关于双重的低速度和显示扩散系数,而控制。这些变化是伴随着减少传播和减少压力的形成纤维和局部粘着斑。分子水平上,记者成纤维细胞显示减少RhoA激活和大量增加的磷酸化细胞外signal-regulated激酶1/2 (ERK1/2)。活动PD98059恢复RhoA激活,细胞骨架组织和细胞的能动性和几乎完全拯救伤口关闭三峡工程成纤维细胞。隔绝KO小鼠显示增加伤口关闭的能力。在三峡工程和加速伤口被推迟老鼠。能动性的一种机制,至少在某种程度上,由ERK1/2。

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