Telocytes enhanced the proliferation, adhesion and motility of endometrial stromal cells as mediated by the ERK pathway in vitro.

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Abstract

motile and invasive capacity of ESCs, which were mediated by the ERK-cyclin-D3 signaling pathway, likely through direct intercellular contacts and/or juxta-paracrine effects; signaling through this axis therefore increased the likelihood of EMs. The enhanced functions of TCs-educated ESCs not only contribute to a deeper understanding of TCs, but also highlight a new concept regarding the physiopathology and therapy of EMs and associated impaired reproductive function.

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