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首页> 外文期刊>Canadian Journal of Physiology and Pharmacology >Stretch-dependent growth and differentiation in vascular smooth muscle: role of the actin cytoskeleton.
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Stretch-dependent growth and differentiation in vascular smooth muscle: role of the actin cytoskeleton.

机译：血管平滑肌的拉伸依赖性生长和分化：肌动蛋白细胞骨架的作用。

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The smooth muscle cells in the vascular wall are constantly exposed to distending forces from the intraluminal pressure. A rise in blood pressure triggers growth of the vessel wall, which is characterized primarily by hypertrophy of smooth muscle cells with maintained differentiation in a contractile phenotype. Growth factor stimulation of dissociated smooth muscle cells, on the other hand, causes proliferative growth with loss of contractility. This type of response is also found in neointima development following angioplasty and in atherosclerotic lesions. An intact tissue environment is therefore critical for preserved differentiation. Recent advances point to a role of actin polymerization in the expression of smooth muscle differentiation marker genes, in concert with serum response factor (SRF) and cofactors, such as myocardin. Stretch of intact venous smooth muscle activates Rho and inhibits the actin filament severing factor cofilin, resulting in increased actin polymerization. Concomitantly, the rates of synthesis of SRF-regulated differentiation markers, such as SM22alpha, calponin, and alpha-actin, are increased. This increase in differentiation signals is parallel with activation of the mitogen-activated protein (MAP) kinase pathway. Thus stretch-induced growth in a maintained contractile phenotype occurs by dual activation of signal pathways regulating both growth and differentiation. A current challenge is to identify sites of crosstalk between these pathways in intact smooth muscle tissue.
机译：血管壁中的平滑肌细胞不断受到来自腔内压力的扩张力的作用。血压升高触发血管壁的生长，其特征主要在于平滑肌细胞肥大，并在收缩表型中保持分化。另一方面，生长因子对解离的平滑肌细胞的刺激导致增殖性生长，而收缩力下降。在血管成形术后的新内膜发育和动脉粥样硬化病变中也发现了这种类型的反应。因此，完整的组织环境对于保持分化至关重要。最近的进展表明肌动蛋白聚合在平滑肌分化标记基因的表达中的作用，与血清反应因子（SRF）和辅助因子（如心肌素）协同作用。伸展完整的静脉平滑肌可激活Rho并抑制肌动蛋白丝切断因子cofilin，从而导致肌动蛋白聚合增加。同时，增加了SRF调节的分化标记（例如SM22α，钙蛋白和α-肌动蛋白）的合成速率。分化信号的这种增加与有丝分裂原激活蛋白（MAP）激酶途径的激活平行。因此，通过调控生长和分化的信号途径的双重激活，在维持的收缩表型中发生拉伸诱导的生长。当前的挑战是在完整的平滑肌组织中识别这些途径之间的串扰位点。

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