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首页> 外文期刊>Journal of Cellular Physiology >Elevated transforming growth factor signaling activation in -actin-knockout mouse embryonic fibroblasts enhances myofibroblast features
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Elevated transforming growth factor signaling activation in -actin-knockout mouse embryonic fibroblasts enhances myofibroblast features

机译：转化生长因子信号升高激活-actin-knockout老鼠胚胎成纤维细胞增强myofibroblast特性

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摘要

Signaling by the transforming growth factor- (TGF-) is an essential pathway regulating a variety of cellular events. TGF- is produced as a latent protein complex and is required to be activated before activating the receptor. The mechanical force at thecell surface is believed to be a mechanism for latent TGF- activation. Using -actin null mouse embryonic fibroblasts as a model, in which actin cytoskeleton and cell-surface biophysical features are dramatically altered, we reveal increased TGF-1 activation and the upregulation of TGF- target genes. In -actin null cells, we show evidence that the enhanced TGF- signaling relies on the active utilization of latent TGF-1 in the cell culture medium. TGF- signaling activation contributes to the elevated reactive oxygen speciesproduction, which is likely mediated by the upregulation of Nox4. The previously observed myofibroblast phenotype of -actin null cells is inhibited by TGF- signaling inhibition, while the expression of actin cytoskeleton genes and angiogenic phenotype are not affected. Together, our study shows a scenario that the alteration of the actin cytoskeleton and the consequent changes in cellular biophysical features lead to changes in cell signaling process such as TGF- activation, which in turn contributes to the enhanced myofibroblast phenotype.
机译：转化生长因子-信号(TGF)是一个重要的途径调节各种各样的细胞活动。潜在的蛋白质复杂和需要激活之前激活受体。机械力被认为在细胞表面是一个潜在的TGF -激活的机制。使用零小鼠胚胎成纤维细胞,肌动蛋白肌动蛋白细胞骨架和一个模型,细胞表面生物物理特性戏剧性的改变,我们揭示TGF-1增加激活和upregulation TGF -目标基因。增强的TGF -信号依赖于积极利用潜在TGF-1细胞培养基。导致了活性氧升高speciesproduction,这可能是由Nox4 upregulation。myofibroblast肌动蛋白空细胞的表型抑制了TGF -信号抑制,而肌动蛋白细胞骨架基因的表达血管生成表型不受影响。我们的研究显示了一个场景的改变肌动蛋白细胞骨架的变化在细胞生物物理特性导致的变化在细胞信号传导过程中如TGF -激活,进而导致的增强myofibroblast表型。

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