Association of placental PPARα/γ and miR-27b expression with macrosomia in healthy pregnancy

Pediatr Res. 2023 Jan;93(1):267-273. doi: 10.1038/s41390-022-02072-1. Epub 2022 Apr 22.

Abstract

Background: Peroxisomal proliferator-activated receptors (PPARs) and microRNAs (miRNAs) play important roles in the development of fetuses, whereas expression changes of PPARs and three miRNAs (miR-17, miR-27b and miR-34a) and whether these miRNAs regulate PPARs in non-GDM macrosomia placenta is unclear.

Methods: A case-control study was performed to collect information and placental tissues on mothers and newborns of non-GDM macrosomia and normal-birth-weight infants. In vitro HTR8-SVneo cellular model was used to detect the effects of miRNAs on PPARs expression. Quantitative real-time PCR (qRT-PCR) and western blot was applied to examine the expression levels of PPARs, miR-17, miR-27b, and miR-34a in placental tissues and cells.

Results: The PPARα/γ mRNA and protein levels were significantly up-regulated and miR-27b was down-regulated in the placenta of macrosomia group compared with in the control group, while no difference was observed in PPARβ, miR-17, and miR-34a. After adjusting for confounding factors, low miR-27b and high PPARα/γ mRNA expression still increased the risk of macrosomia. The PPARα/γ protein levels presented a corresponding decrease or increase when cells were transfected with miR-27b mimic or inhibitor.

Conclusions: Placental PPARα/γ and miR-27b expression were associated with non-GDM macrosomia and miR-27b probably promotes the occurrence of non-GDM macrosomia by regulating PPARα/γ protein.

Impact: Low miR-27b and high PPARα/γ mRNA expression in the placenta were associated with higher risk of macrosomia. In vitro HTR8-SVneo cell experiment supported that miR-27b could negatively regulate the expression of PPARα and PPARγ protein. MiR-27b was probably involved in non-GDM macrosomia through negative regulation of PPARα/γ protein.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Case-Control Studies
  • Female
  • Fetal Macrosomia / genetics
  • Fetal Macrosomia / metabolism
  • Humans
  • Infant, Newborn
  • MicroRNAs* / genetics
  • MicroRNAs* / metabolism
  • PPAR alpha / genetics
  • PPAR alpha / metabolism
  • Placenta* / metabolism
  • Pregnancy
  • RNA, Messenger / metabolism

Substances

  • PPAR alpha
  • MicroRNAs
  • RNA, Messenger