miR-183-5p regulates uterine receptivity and enhances embryo implantation

in Journal of Molecular Endocrinology
View More View Less
  • 1 The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
  • 2 Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
  • 3 Department of Zoology, University of Swabi, Anbar, Khyber Pakhtunkhwa, Pakistan
  • 4 Department of Reproductive Endocrinology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
  • 5 The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

Correspondence should be addressed to H-F Huang or J-Z Sheng: huanghefg@hotmail.com or shengjz@zju.edu.cn

*(R Akbar and K Ullah contributed equally to this work)

Restricted access

Receptive endometrium is a prerequisite for successful embryo implantation, and it follows that poor endometrial receptivity is a leading cause of implantation failure. miRNAs play important roles as epigenetic regulators of endometrial receptivity and embryo implantation through post-transcriptional modifications. However, the mechanisms of action of many miRNAs are poorly understood. In this study, we investigated the role of the miR-183 family, comprising three miRNAs (miR-183-5p, miR-182-5p, and miR-96-5p) in endometrial receptivity and embryo implantation. The miR-183 family shows estrogen-dependent upregulation in endometrial Ishikawa (IK) cells. The miR-183 family also has a positive role in migration and proliferation of IK cells. Furthermore, JAr spheroid attachment experiments show that attachment rates were significantly decreased after treatment of IK cells with inhibitors for miR-183-5p and miR-182-5p and increased after treatment with miR-183-5p-mimic and miR-96-5p-mimic, respectively. The downstream analysis shows that catenin alpha 2 (CTNNA2) is a potential target gene for miR-183-5p, and this was confirmed in luciferase reporter assays. An in vivo mouse pregnancy model shows that inhibition of miR-183-5p significantly decreases embryo implantation rates and increases CTNNA2 expression. Downregulation of CTNNA2 in endometrial cells by miR-183-5p may be significant in mediating estrogenic effects on endometrial receptivity. In conclusion, miR-183-5p and the CTNNA2 gene may be potential biomarkers for endometrial receptivity and may be useful diagnostic and therapeutic targets for successful embryo implantation.

Supplementary Materials

    • Sequence of Inhibitors and mimics
    • Primers sequence for Q-PCR
    • h-CTNNA2 (NM_001282598.1 3’UTR: 1-792)-WT


      Society for Endocrinology

Sept 2018 onwards Past Year Past 30 Days
Abstract Views 1542 1542 215
Full Text Views 94 94 4
PDF Downloads 71 71 7