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首页> 外文期刊>Journal of Cellular Physiology >Cellular and Molecular Mechanisms of Phenotypic Switch in Gastrointestinal Smooth Muscle
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Cellular and Molecular Mechanisms of Phenotypic Switch in Gastrointestinal Smooth Muscle

机译：表型的细胞和分子机制开关在胃肠道平滑肌

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As a general rule, smooth muscle cells (SMC) are able to switch from a contractile phenotype to a less mature synthetic phenotype. This switch is accompanied by a loss of differentiation with decreased expression of contractile markers, increased proliferation as well as the synthesis and the release of several signaling molecules such as pro-inflammatory cytokines, chemotaxis-associated molecules, and growth factors. This SMC phenotypic plasticity has extensively been investigated in vascular diseases, but interest is also emerging in the field of gastroenterology. It has in fact been postulated that altered microenvironmental conditions, including the composition of microbiota, could trigger the remodeling of the enteric SMC, with phenotype changes and consequent alterations of contraction and impairment of gut motility. Several molecular actors participate in this phenotype remodeling. These include extracellular molecules such as cytokines and extracellular matrix proteins, as well as intracellular proteins, for example, transcription factors. Epigenetic control mechanisms and miRNA have also been suggested to participate. In this review key roles and actors of smooth muscle phenotypic switch, mainly in GI tissue, are described and discussed in the light of literature data available so far. J. Cell. Physiol. 231: 295-302, 2016. (c) 2015 Wiley Periodicals, Inc.
机译：作为一般规则,平滑肌细胞(SMC)可以切换从一个收缩表型不成熟的合成表型。伴随着失去分化减少收缩标记的表达,扩散以及合成增加和一些信号分子的释放如促炎细胞因子,chemotaxis-associated分子,和增长的因素。广泛的血管被调查疾病,但也出现了利益的胃肠病学领域。假定改变微环境条件,包括的构成微生物群,可能引发的重构肠SMC表型变化和随之收缩和改变损伤的肠道蠕动。演员参与这个表型重建。这些包括细胞外分子等细胞因子和细胞外基质蛋白胞内蛋白,例如,转录因子。机制和microrna也被建议参与。主要在胃肠道平滑肌的表型转换组织、描述和讨论的光到目前为止的文献数据。杂志。231:295 - 302年,2016年。期刊、公司。

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