miR-183-5p regulates uterine receptivity and enhances embryo implantation
Autor: | Yi Cheng, Jian-Zhong Sheng, Hai-Yan Pang, Rubab Akbar, Kamran Ullah, He-Feng Huang, Qijing Wang, Tanzil Ur Rahman, Lu Yang Jin |
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Rok vydání: | 2020 |
Předmět: |
Male
0301 basic medicine Down-Regulation 030209 endocrinology & metabolism Biology Endometrium Andrology Mice 03 medical and health sciences 0302 clinical medicine Endocrinology Downregulation and upregulation Cell Movement Pregnancy In vivo microRNA medicine Animals Humans Embryo Implantation Epigenetics Molecular Biology Gene Cells Cultured Cell Proliferation Mice Inbred ICR Uterus Embryo MicroRNAs HEK293 Cells 030104 developmental biology medicine.anatomical_structure Catenin Female Biomarkers alpha Catenin |
Zdroj: | Journal of Molecular Endocrinology. 64:43-52 |
ISSN: | 1479-6813 0952-5041 |
DOI: | 10.1530/jme-19-0184 |
Popis: | 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. |
Databáze: | OpenAIRE |
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