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Telocytes enhanced in vitro decidualization and mesenchymal-epithelial transition in endometrial stromal cells via Wnt/β-catenin signaling pathway

机译:通过Wnt /β-catenin信号通路在子宫内膜基质细胞中增强了体外脱链和间充质的上皮性转变的体外丧失丧失

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摘要

Decidualization of endometrial stromal cells (ESCs) is essential for preparing endometrium for embryo implantation. Telocytes (TCs), a novel type of interstitial cell, exist in the female reproductive tract and participate in the pathophysiology of diseases. This study further investigates the hypothesis that TCs, a source of Wnt, modulates decidualization and MET in ESCs. We had observed differential expression of Wnt ligands in primary mice ESCs and TCs by qPCR. TCM-induced decidualization and MET was assessed in ESCs. Changes in markers for decidualization (cyclin-D3, desmin, d/tPRP), stromal cells (N-cadherin), epithelial cells (E-cadherin), and the Wnt/β-catenin pathway (β-catenin, FOXO1) were quantified by western blot and RT-PCR. β-catenin knockdown in ESCs decreased the degree of TCM-induced decidualization and MET, with significantly reversed expression profiles ( < 0.05). This is the first study to show that TCs can enhance decidualization and MET in ESCs through the Wnt/β-catenin signaling-pathway. Therefore, we describe a promising cell therapy for gynecological conditions and related reproductive problems associated with defective decidualization.
机译:子宫内膜基质细胞(ESC)的蜕膜化对于制备用于胚胎植入的子宫内膜是必不可少的。电轭(TCS)是一种新型的间质细胞,存在于女性生殖道中,并参与疾病的病理生理学。本研究进一步研究了TCS,WNT的来源,调节DeCiAnization并在ESC中满足的假设。我们通过QPCR观察到原发性小鼠ESC和TCS中WNT配体的差异表达。在ESC评估中医诱导的DeCidualization和Met。量化的标志物(Cyclin-D3,Desmin,D / TprP),基质细胞(N-钙粘蛋白),上皮细胞(E-Cadherin)和Wnt /β-catenin途径(β-catenin,Foxo1)的变化量通过Western印迹和RT-PCR。 β-catenin在ESC的敲低下降了TCM诱导的Drocualization和满足的程度,具有显着反转的表达曲线(<0.05)。这是第一项研究表明TCS可以通过WNT /β-catenin信号传导通路在ESC中增强蜕皮化并在ESC中满足。因此,我们描述了对妇科病症的有前途的细胞疗法和与缺陷蜕皮化相关的相关生殖问题。

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