Promotion of trophoblast invasion by lncRNA MVIH through inducing Jun-B

J Cell Mol Med. 2018 Feb;22(2):1214-1223. doi: 10.1111/jcmm.13400. Epub 2017 Oct 30.

Abstract

Preeclampsia (PE), a pregnancy-specific disorder, is associated with impaired uterine spiral artery remodelling, which is related to the dysfunction of trophoblast cells. Lately, mounting evidence has indicated that aberrant expression of long non-coding RNAs (lncRNAs) is associated with various human diseases. The lncRNA MVIH transcript has been shown to decrease the severity of several diseases. However, the biological function of MVIH, which is down-regulated in placental tissues in PE, has not yet been clarified. Here, we report that MVIH may act as a vital factor in the pathogenesis of PE. In this study, functional analysis revealed that the silencing of MVIH expression via transfection with small interfering RNA (siRNAs) inhibited cell growth, migration, invasion, and angiogenesis in various trophoblast cell lines, and stimulation with MVIH could promote these functions. Mass spectrometry analysis revealed that MVIH could modulate Jun-B protein expression, which has been reported to potentially regulate cell growth and angiogenesis. Further cotransfection assays were performed, revealing that MVIH and Jun-B have a synergistic effect on the regulation of angiogenesis and cell proliferation. Taking these findings together, MVIH could be associated with PE and may be a candidate biomarker for its diagnosis and treatment.

Keywords: MVIH; Jun-B; Preeclampsia; long non-coding RNAs.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cell Line
  • Cell Movement
  • Cell Proliferation
  • Down-Regulation / genetics
  • Female
  • Human Umbilical Vein Endothelial Cells / metabolism
  • Humans
  • Neovascularization, Physiologic
  • Placenta / metabolism
  • Pre-Eclampsia / genetics
  • Pre-Eclampsia / pathology
  • Pregnancy
  • RNA, Long Noncoding / genetics
  • RNA, Long Noncoding / metabolism*
  • Transcription Factors / genetics
  • Transcription Factors / metabolism*
  • Trophoblasts / metabolism*
  • Trophoblasts / pathology*
  • Up-Regulation / genetics

Substances

  • JunB protein, human
  • RNA, Long Noncoding
  • Transcription Factors