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MiR199a is implicated in embryo implantation by regulating Grb10 in rat
Hong-Fei Xia1, Jing-Li Cao, Xiao-Hua Jin
1Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing 100081, China.
Reproduction (Cambridge, England)
|October 24, 2013
Summary
MicroRNA 199a (miR199a) is upregulated in the receptive rat uterus, regulating embryo implantation by inhibiting cell proliferation and targeting Grb10. This study elucidates miR199a's role in uterine receptivity.
Area of Science:
- Reproductive Biology
- Molecular Endocrinology
- Genetics
Background:
- MicroRNA (miRNA) microarray analysis previously identified differential expression of miR199a in rat uteri during prereceptive and receptive phases.
- The specific function of miR199a in rat embryo implantation remained uncharacterized.
Purpose of the Study:
- To investigate the role of miR199a in rat uterine receptivity and embryo implantation.
- To determine the regulatory mechanisms and downstream targets of miR199a during uterine preparation for pregnancy.
Main Methods:
- Northern blot and in situ hybridization to analyze miR199a expression levels and localization in rat uteri across different gestational stages.
- Uterine analysis in pseudopregnant, delayed implantation, and experimentally induced decidualization models.
- Hormonal treatments (17β-estradiol, progesterone) and in vitro/in vivo gain and loss-of-function studies on endometrial stromal cells.
- Analysis of miR199a interaction with growth factor receptor-bound protein 10 (Grb10) using 3'UTR binding assays and immunostaining.
Main Results:
- miR199a expression is significantly elevated in rat uteri during gestation days 5-6, localized to the stroma/decidua, and upregulated during decidualization.
- Hormonal treatments with 17β-estradiol or progesterone decreased miR199a levels.
- Gain of function for miR199a inhibited stromal cell proliferation and promoted apoptosis, while loss of function had opposite effects.
- miR199a directly targets the 3'UTR of Grb10, inhibiting its translation, with inverse expression patterns observed in vivo.
Conclusions:
- Upregulation of miR199a in the rat uterus during the receptive phase is triggered by blastocyst activation and uterine decidualization.
- miR199a plays a crucial role in regulating uterine stromal cell proliferation and apoptosis, contributing to embryo implantation.
- The inhibitory effect of miR199a on cell proliferation is partly mediated by targeting the imprinted gene Grb10.
