Platelets drive smooth muscle metaplasia and fibrogenesis in endometriosis through epithelial–mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation

Zhang Q, Qi Zhang, Duan J, Jie Duan, Liu X, Xishi Liu, Sun-Wei Guo, Sun‐Wei Guo, Guo SW
Molecular and cellular endocrinology · 2016 · vol. 428 , pp. 1–16 · doi:10.1016/j.mce.2016.03.015 · PMID:26992563 · W2299003422
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Platelets induce smooth muscle metaplasia and fibrogenesis in endometriosis by promoting epithelial-mesenchymal transition and fibroblast-to-myofibroblast transdifferentiation.

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Abstract

Smooth muscle metaplasia (SMM) and fibrotic tissues are frequently seen in endometriotic lesions, yet the mechanisms underlying their formation are poorly understood. In this study, we investigated the roles of activated platelets in driving epithelial-mesenchymal transition (EMT) and fibroblast-to-myofibroblast transdifferentiation (FMT) in endometriosis. Through in vitro experimentations, we found that activated platelets, through the release of TGF-β1 and the induction of TGF-β/Smad signaling pathway, promoted EMT and FMT in endometriosis, resulting in increased cell contractility, collagen production, and ultimately to fibrosis. TGF-β blockade reversed these processes. Prolonged exposure of endometriotic stromal cells to activated platelets induced increased expression of α-SMA as well as markers of differentiated smooth muscle cells. Consequently, endometriotic lesions and their microenvironment contain all the necessary molecular machinery to promote SMM and fibrogenesis. Our results suggest that endometriotic lesions are wounds that undergo repeated injury and healing, highlighting the importance of platelets in the development of endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Blood Platelets Cell Transdifferentiation Endometriosis Epithelial-Mesenchymal Transition Muscle, Smooth Myofibroblasts Actins Actins Adult Antigens, CD Antigens, CD Blood Platelets Cadherins Cadherins Cell Movement Cell Shape Collagen Collagen Endometriosis Epithelial Cells

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. [ expand to 2 hops ] — adds papers reached through this work's immediate citers/citees. Heavier; up to 60 extra dots.

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