Gestational loss and growth restriction by angiogenic defects in placental growth factor transgenic mice

Arterioscler Thromb Vasc Biol. 2014 Oct;34(10):2276-82. doi: 10.1161/ATVBAHA.114.303693. Epub 2014 Aug 21.

Abstract

Objective: Angiogenesis is an important biological process during development, reproduction, and in immune responses. Placental growth factor (PlGF) is a member of vascular endothelial growth factor that is critical for angiogenesis and vasculogenesis. We generated transgenic mice overexpressing PlGF in specifically T cells using the human CD2-promoter to investigate the effects of PlGF overexpression.

Approach and results: Transgenic mice were difficult to obtain owing to high lethality; for this reason, we investigated why gestational loss occurred in these transgenic mice. Here, we report that placenta detachment and inhibition of angiogenesis occurred in PlGF transgenic mice during the gestational period. Moreover, even when transgenic mice were born, their growth was restricted.

Conclusions: Conclusively, PlGF overexpression prevents angiogenesis by inhibiting Braf, extracellular signal-regulated kinase activation, and downregulation of HIF-1α in the mouse placenta. Furthermore, it affected regulatory T cells, which are important for maintenance of pregnancy.

Keywords: BRAF kinases; extracellular signal-regulated kinases; miscarriage; placenta growth factor; regulatory T-cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Body Weight
  • CD2 Antigens / genetics
  • Cells, Cultured
  • Extracellular Signal-Regulated MAP Kinases / metabolism
  • Female
  • Fetal Death / genetics
  • Fetal Death / metabolism*
  • Fetal Death / physiopathology
  • Fetal Growth Retardation / genetics
  • Fetal Growth Retardation / metabolism*
  • Fetal Growth Retardation / physiopathology
  • Gestational Age
  • Humans
  • Hypoxia-Inducible Factor 1, alpha Subunit / metabolism
  • Litter Size
  • Mice
  • Mice, Inbred C57BL
  • Mice, Transgenic
  • Neovascularization, Physiologic*
  • Placenta / blood supply*
  • Placenta / metabolism*
  • Placenta Growth Factor
  • Pregnancy
  • Pregnancy Proteins / genetics
  • Pregnancy Proteins / metabolism*
  • Promoter Regions, Genetic
  • Proto-Oncogene Proteins B-raf / metabolism
  • Signal Transduction
  • T-Lymphocytes, Regulatory / metabolism*
  • Up-Regulation

Substances

  • CD2 Antigens
  • Hif1a protein, mouse
  • Hypoxia-Inducible Factor 1, alpha Subunit
  • PGF protein, human
  • Pgf protein, mouse
  • Pregnancy Proteins
  • Placenta Growth Factor
  • Braf protein, mouse
  • Proto-Oncogene Proteins B-raf
  • Extracellular Signal-Regulated MAP Kinases