Evidence that miR-133a causes recurrent spontaneous abortion by reducing HLA-G expression.

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  • Author(s): Wang X;Wang X; Li B; Wang J; Lei J; Liu C; Ma Y; Zhao H
  • Source:
    Reproductive biomedicine online [Reprod Biomed Online] 2012 Oct; Vol. 25 (4), pp. 415-24. Date of Electronic Publication: 2012 Jul 20.
  • Publication Type:
    Journal Article; Research Support, Non-U.S. Gov't
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: Netherlands NLM ID: 101122473 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1472-6491 (Electronic) Linking ISSN: 14726483 NLM ISO Abbreviation: Reprod Biomed Online Subsets: MEDLINE
    • Publication Information:
      Publication: <2009->: Amsterdam : Elsevier
      Original Publication: Cambridge, UK : Reproductive Healthcare Ltd.
    • Subject Terms:
      Down-Regulation* ; Up-Regulation*; Abortion, Habitual/*metabolism ; Chorionic Villi/*metabolism ; HLA-G Antigens/*metabolism ; MicroRNAs/*metabolism; 3' Untranslated Regions ; Abortion, Habitual/genetics ; Adult ; Cell Line ; China ; Chorionic Villi Sampling ; Comparative Genomic Hybridization ; Female ; Genes, Reporter ; HLA-G Antigens/genetics ; Humans ; Karyotype ; MicroRNAs/genetics ; Mutant Proteins/metabolism ; Pregnancy ; Pregnancy Trimester, First ; Recombinant Proteins/metabolism
    • Abstract:
      Human leukocyte antigen (HLA)-G is thought to confer fetal-maternal tolerance and play a crucial role in ensuring a successful pregnancy. There is increasing evidence that HLA-G is regulated at the post-transcriptional level. This study investigated the role of miR-133a in regulating HLA-G expression and the pathogenesis of recurrent spontaneous abortion (RSA). Twelve patients (25-30 years) with RSA at 7 gestational weeks were screened by array-based comparative genome hybridization: 16.7% were found to have an abnormal karyotype and all induced abortion (IA) patients had normal karyotype. The villi of RSA and IA patients with normal karyotype were further screened by miRNA microarrays. Multi-software prediction and real-time PCR confirmed that miR-133a was most likely to bind to HLA-G 3' untranscribed region (UTR). Relevance analysis showed that, compared with IA villi, miR-133a was greatly overexpressed in RSA villi with normal karyotype (P<0.01), but not in abnormal RSA villi. A luciferase reporter assay suggested that miR-133a interacted with HLA-G 3' UTR. Overexpression of miR-133a in JEG-3 cells decreased HLA-G expression at the protein level, with no effect on mRNA. These findings provide strong evidence that miR-133a regulates HLA-G expression by reducing translation and is involved in the pathogenesis of RSA.
      (Copyright © 2012 Reproductive Healthcare Ltd. Published by Elsevier Ltd. All rights reserved.)
    • Accession Number:
      0 (3' Untranslated Regions)
      0 (HLA-G Antigens)
      0 (MIRN133 microRNA, human)
      0 (MicroRNAs)
      0 (Mutant Proteins)
      0 (Recombinant Proteins)
    • Publication Date:
      Date Created: 20120811 Date Completed: 20130301 Latest Revision: 20201219
    • Publication Date:
      20231215
    • Accession Number:
      10.1016/j.rbmo.2012.06.022
    • Accession Number:
      22877943