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Collagen gel contractility is enhanced in human endometriotic stromal cells: a possible mechanism underlying the pathogenesis of endometriosis-associated fibrosis

机译:人体子宫内膜异位基质细胞中胶原蛋白凝胶的收缩性增强:子宫内膜异位症相关纤维化发病机制的潜在机制

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BACKGROUND Excessive fibrosis is frequently associated with endometriosis. To evaluate the involvement of the extracellular matrix contractility of endometriotic stromal cells (ECSCs) in the pathogenesis of endometriosis-associated fibrosis, we compared the collagen gel contractility of cultured ECSCs with that of normal endometrial stromal cells. To clarify the mechanism underlying collagen gel contraction by ECSCs, we also evaluated the effect of (+)-(R)-trans-4-(1-aminoethyl)-N-(4-pyridyl) cyclohexanecarboxamide dihydrochloride, monohydrate (Y-27632), a selective Rho-associated coiled-coil-forming protein kinase (ROCK) inhibitor, on the collagen gel contraction by ECSCs.
机译:背景技术过度纤维化通常与子宫内膜异位症相关。为了评估子宫内膜异位基质细胞(ECSCs)的胞外基质收缩在子宫内膜异位症相关纤维化发病机理中的作用,我们比较了培养的ECSCs和正常子宫内膜基质细胞的胶原凝胶收缩能力。为了阐明ECSC胶原蛋白凝胶收缩的基本机制,我们还评估了(+)-(R)-反式-4-(1-氨基乙基)-N-(4-吡啶基)环己烷甲酰胺二盐酸盐一水合物(Y-27632)的作用),一种选择性的Rho相关的卷曲螺旋形成蛋白激酶(ROCK)抑制剂,可抑制ECSC的胶原凝胶收缩。

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