miR-483 is downregulated in pre-eclampsia via targeting insulin-like growth factor 1 (IGF1) and regulates the PI3K/Akt/mTOR pathway of endothelial progenitor cells

J Obstet Gynaecol Res. 2021 Jan;47(1):63-72. doi: 10.1111/jog.14412. Epub 2020 Sep 28.

Abstract

Aim: Pre-eclampsia is a serious pregnancy-specific disease with an incidence of 9.4%. MicroRNAs play a key role in regulating factors in pre-eclampsia, but related research is still limited. This study aims to reveal the role and potential mechanisms of miR-483 in pre-eclampsia.

Methods: miR-483 was detected in venous blood, umbilical cord blood and placental tissue of pre-eclampsia patients by Real-time Quantitative polymerase chain reaction (qRT-PCR). Insulin-like growth factor (IGF1) and miR-483 were detected by qRT-PCR and western blot in endothelial progenitor cells isolated from fetal umbilical cord blood. miR-483 was overexpressed and inhibited to detect changes of IGF1 and PI3K/Akt/mTOR pathway in endothelial progenitor cells by qRT-PCR and western blot.

Results: miR-483 was downregulated in venous blood, umbilical cord blood and placental tissue of pre-eclampsia patients. In endothelial progenitor cells, overexpression of miR-483 inhibited the expression of IGF1, and inhibition of miR-483 promoted the expression of IGF1. miR-483 regulates the expression of PI3K, Akt, and mTOR in endothelial progenitor cells.

Conclusion: miR-483 is downregulated in pre-eclampsia and regulates endothelial progenitor cells by targeting IGF1. miR-483 is a potential alternative for diagnosing and treating pre-eclampsia.

Keywords: IGF1; PI3K/Akt/mTOR; miR-483; pre-eclampsia.

MeSH terms

  • Cell Proliferation
  • Endothelial Progenitor Cells*
  • Female
  • Humans
  • Insulin-Like Growth Factor I / genetics
  • MicroRNAs* / genetics
  • Phosphatidylinositol 3-Kinases
  • Placenta
  • Pre-Eclampsia* / genetics
  • Pregnancy
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases

Substances

  • IGF1 protein, human
  • MIRN483 microRNA, human
  • MicroRNAs
  • Insulin-Like Growth Factor I
  • MTOR protein, human
  • Proto-Oncogene Proteins c-akt
  • TOR Serine-Threonine Kinases