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Potential role of microRNAs in mammalian female fertility.

Authors :
Tesfaye D
Salilew-Wondim D
Gebremedhn S
Sohel MM
Pandey HO
Hoelker M
Schellander K
Source :
Reproduction, fertility, and development [Reprod Fertil Dev] 2016 Jan; Vol. 29 (1), pp. 8-23.
Publication Year :
2016

Abstract

Since the first evidence for the involvement of microRNAs (miRNAs) in various reproductive processes through conditional knockout of DICER, several studies have been conducted to investigate the expression pattern and role of miRNAs in ovarian follicular development, oocyte maturation, embryo development, embryo-maternal communication, pregnancy establishment and various reproductive diseases. Although advances in sequencing technology have fuelled miRNA studies in mammalian species, the presence of extracellular miRNAs in various biological fluids, including follicular fluid, blood plasma, urine and milk among others, has opened a new door in miRNA research for their use as diagnostic markers. This review presents data related to the identification and expression analysis of cellular miRNA in mammalian female fertility associated with ovarian folliculogenesis, oocyte maturation, preimplantation embryo development and embryo implantation. In addition, the relevance of miRNAs to female reproductive disorders, including polycystic ovary syndrome (PCOS), endometritis and abnormal pregnancies, is discussed for various mammalian species. Most importantly, the mechanism of release and the role of extracellular miRNAs in cell-cell communication and their potential role as non-invasive markers in female fertility are discussed in detail. Understanding this layer of regulation in female reproduction processes will pave the way to understanding the genetic regulation of female fertility in mammalian species.

Details

Language :
English
ISSN :
1448-5990
Volume :
29
Issue :
1
Database :
MEDLINE
Journal :
Reproduction, fertility, and development
Publication Type :
Academic Journal
Accession number :
28278789
Full Text :
https://doi.org/10.1071/RD16266