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

in Journal of Molecular Endocrinology
Authors:
Rubab Akbar The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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Kamran Ullah The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China
Department of Zoology, University of Swabi, Anbar, Khyber Pakhtunkhwa, Pakistan

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Tanzil Ur Rahman The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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Yi Cheng The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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Hai-Yan Pang The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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Lu-Yang Jin The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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Qi-Jing Wang The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Reproductive Endocrinology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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He-Feng Huang The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
The International Peace Maternity and Child Health Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, China

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Jian-Zhong Sheng The Key Laboratory of Reproductive Genetics (Zhejiang University), Ministry of Education
Department of Pathology and Pathophysiology, School of Medicine, Zhejiang University, Hangzhou, Zhejiang, China

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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)

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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

 

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