Format

Send to:

Choose Destination
See comment in PubMed Commons below
FEBS Lett. 2014 Feb 14;588(4):574-83. doi: 10.1016/j.febslet.2013.12.026. Epub 2014 Jan 18.

MiR-98 is involved in rat embryo implantation by targeting Bcl-xl.

Author information

  • 1Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing 100081, China; Graduate School, Peking Union Medical College, Beijing, China. Electronic address: hongfeixia@126.com.
  • 2Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing 100081, China.
  • 3Haidian Maternal & Child Health Hospital, Beijing, China.
  • 4Reproductive and Genetic Center of National Research Institute for Family Planning, Beijing 100081, China; Graduate School, Peking Union Medical College, Beijing, China. Electronic address: genetic@263.net.cn.

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microarray analysis we found that miR-98 is differentially expressed in rat uteri during the peri-implantation period (unpublished data).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.

Copyright © 2014 Federation of European Biochemical Societies. Published by Elsevier B.V. All rights reserved.

KEYWORDS:

Bcl-xl; Embryo implantation; Rat; Uterus; miR-98

PMID:
24444606
[PubMed - indexed for MEDLINE]
Free full text
PubMed Commons home

PubMed Commons

0 comments
How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for Elsevier Science
    Loading ...
    Write to the Help Desk