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Reprod Sci. 2016 Mar;23(3):386-94. doi: 10.1177/1933719115602768. Epub 2015 Sep 21.

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

Author information

1
Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China Currently affiliated with the Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
2
Department of Orthopedics, The Second Affiliated Hospital of Zhejiang University School of Medicine, Hangzhou, China.
3
Department of Obstetrics and Gynecology, Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
4
Department of Pharmacy, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
5
Department of Pathology, Zhujiang Hospital, Southern Medical University, Guangzhou, China.
6
Department of Obstetrics and Gynecology, Zhujiang Hospital, Southern Medical University, Guangzhou, China heyuanli310@126.com.

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.

KEYWORDS:

TGF-β signaling; agomir-29b; endometrial fibrosis; epithelial–mesenchymal transition; intrauterine adhesions

PMID:
26392347
DOI:
10.1177/1933719115602768
[Indexed for MEDLINE]

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