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MicroRNA-29b Inhibits Endometrial Fibrosis by Regulating the Sp1-TGF-β1/Smad-CTGF Axis in a Rat Model.

Abstract
Intrauterine adhesions (IUAs), which are characterized by endometrial fibrosis, increase the risk of secondary infertility and recurrent miscarriage. MicroRNA-29 (miR-29) is a potent inhibitor of TGF-β1/Smad signaling. In this study, we investigated the therapeutic potential of agomir-29b, an miR-29b mimic, in endometrial fibrosis induced by dual injury (uterine curettage and lipopolysaccharide treatment) in a rat model of IUA and explored the underlying mechanism. We found that injured rats developed endometrial fibrosis characterized by increased COL1A1 and α-smooth muscle actin expression and decreased E-cadherin expression, associated with a loss of miR-29b. Overexpression of miR-29b before injury prevented endometrial fibrosis including collagen accumulation and epithelial-mesenchymal transition. Delay of agomir-29b treatment until endometrial fibrosis was established on day 4 also halted the progression of disease. Further experiments indicated that miR-29b inhibited endometrial fibrosis via blockade of the Sp1-TGF-β1/Smad-CTGF pathway. In conclusion, agomir-29b may act as a novel and effective therapeutic agent against IUAs.
AuthorsJingxiong Li, Shaohua Du, Xiujie Sheng, Juan Liu, Bohong Cen, Feng Huang, Yuanli He
JournalReproductive sciences (Thousand Oaks, Calif.) (Reprod Sci) Vol. 23 Issue 3 Pg. 386-94 (Mar 2016) ISSN: 1933-7205 [Electronic] United States
PMID26392347 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't)
Copyright© The Author(s) 2015.
Chemical References
  • CCN2 protein, rat
  • MIRN29 microRNA, mouse
  • MicroRNAs
  • Smad Proteins
  • Sp1 Transcription Factor
  • SP1 protein, human
  • Transforming Growth Factor beta1
  • Connective Tissue Growth Factor
Topics
  • Animals
  • Connective Tissue Growth Factor (physiology)
  • Disease Models, Animal
  • Endometrium (metabolism, pathology)
  • Female
  • Fibrosis (metabolism, pathology)
  • MicroRNAs (biosynthesis)
  • Rats
  • Rats, Sprague-Dawley
  • Smad Proteins (physiology)
  • Sp1 Transcription Factor (physiology)
  • Transforming Growth Factor beta1 (physiology)

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