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Preparation of Rat Serum Suitable for Mammalian Whole Embryo Culture
Published on: August 3, 2014
MiR-98 is involved in rat embryo implantation by targeting Bcl-xl
Hong-Fei Xia1, Xiao-Hua Jin2, Zong-Fu Cao2
1Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing 100081, China; Graduate School, Peking Union Medical College, Beijing, China.
Abstract:
In a previous study, via microRNA microarray analysis we found that miR-98 is differentially expressed in rat uteri during the peri-implantation period (unpublished data). However, the role of miR-98 in rat embryo implantation remains elusive. Here, we found that the level of miR-98 is lower on day 5 and 6 of gestation (g.d. 5-6) than that on g.d. 3-4 and g.d. 7-8 in rat. MiR-98 expression is significantly decreased by delayed implantation. Down-regulation of miR-98 promotes ESC proliferation and inhibits apoptosis. Up-regulation of miR-98 displays opposite effects. Further investigation revealed that miR-98 can bind to the 3'-untranslated region (3'-UTR) of B-cell lymphoma-extra large (Bcl-xl) to inhibit Bcl-xl translation. Collectively, down-regulation of miR-98 in rat uterus during the receptive phase is linked to the increase of cell proliferation via targeting Bcl-xl.
Insights
MicroRNA-98 (miR-98) levels decrease during rat embryo implantation, promoting cell proliferation by targeting B-cell lymphoma-extra large (Bcl-xl). Lower miR-98 expression is linked to increased cell proliferation.
Area of Science:
- Developmental Biology
- Molecular Biology
- Reproductive Biology
Background:
- MicroRNA microarray analysis identified differential expression of miR-98 in rat uteri during the peri-implantation period.
- The specific role of miR-98 in rat embryo implantation was previously unknown.
Purpose of the Study:
- To elucidate the function of miR-98 in rat embryo implantation.
- To investigate the regulatory mechanism of miR-98 during uterine receptivity.
Main Methods:
- Quantification of miR-98 expression levels in rat uteri across different gestational days (g.d. 3-8).
- Assessment of miR-98 expression in delayed implantation models.
- Evaluation of miR-98's effect on endometrial stromal cell (ESC) proliferation and apoptosis.
- Luciferase reporter assays to confirm the binding of miR-98 to the 3'-untranslated region (3'-UTR) of B-cell lymphoma-extra large (Bcl-xl) mRNA.
Main Results:
- miR-98 expression was significantly lower on g.d. 5-6 compared to g.d. 3-4 and g.d. 7-8 in rats.
- Delayed implantation led to a significant decrease in miR-98 expression.
- Down-regulation of miR-98 promoted ESC proliferation and inhibited apoptosis, while up-regulation had opposite effects.
- miR-98 directly targets the 3'-UTR of Bcl-xl, inhibiting its translation.
Conclusions:
- Down-regulation of miR-98 in the rat uterus during the receptive phase correlates with increased cell proliferation.
- The mechanism involves miR-98 targeting and inhibiting the translation of Bcl-xl.
- miR-98 plays a crucial role in regulating uterine cell dynamics during embryo implantation.
