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

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Telocytes enhance decidualization and mesenchymal-epithelial transition in endometrial stromal cells via the Wnt/β-catenin signaling pathway, offering a potential therapy for gynecological conditions associated with defective decidualization.

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Abstract

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 (P < 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.

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last seen: 2026-10-04T09:26:46.659050+00:00