Lentiviral vector-mediated down-regulation of Notch1 in endometrial stem cells results in proliferation and migration in endometriosis

He H, Hong He, Rong Liu, Liu R, Xiong W, Wei Xiong, Pu D, Demin Pu, Shixuan Wang, Wang S, Tian Li, Li Tian, Li T
Molecular and cellular endocrinology · 2016 · vol. 434 , pp. 210–218 · doi:10.1016/j.mce.2016.07.004 · PMID:27389878 · W2461041950
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⚙ AI-generated summary by claude@2026-06, 2026-06-13 ⓘ

This study investigated the effect of lentiviral vector-mediated Notch1 down-regulation in endometrial stem cells and found it promoted cell proliferation and migration, offering insights into endometriosis mechanisms.

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Abstract

The recent characterization of stem/progenitor cells in the endometrium has shed new light for pathogenesis of endometriosis. The present study was undertaken to investigate the role of Notch1, known as a cell fate regulator, in the mechanism of endometriosis. Influence of Notch1 on endometrial stem cells proliferation and migration was evaluated by knocking down Notch1 expression using shRNA. Furthermore, human endometrial stromal and epithelial stem cells with or without LV-Notch1-shRNA were injected into the peritoneal cavity of nude mice, to assess the in vivo effects of a specific antagonist of Notch1 on the progression of endometriosis. The results showed that LV-Notch1-shRNA led to a significant decline of clonogenicity and migration in human endometrial stem cells in vitro, as well as the size of endometriotic lesions in murine models. These data provide evidence that specific inhibition of Notch1 alters endometriotic tissue growth and progression, and may represent a promising potential therapeutic avenue.

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Condition tags

endometriosis

MeSH descriptors

Down-Regulation Endometriosis Receptor, Notch1 Stem Cells Adult Animals Cell Movement Cell Proliferation Disease Models, Animal Endometriosis Female Gene Knockdown Techniques Humans Lentivirus Lentivirus Mice Mice, Nude Receptor, Notch1 Signal Transduction Stem 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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