Colony-stimulating factor-1 (CSF-1) expression in the uteroplacental unit of mice with spontaneous and induced pregnancy loss

Clin Exp Immunol. 1999 Sep;117(3):540-9. doi: 10.1046/j.1365-2249.1999.00986.x.

Abstract

CSF-1 plays an important role in female reproduction and normal embryo development. To understand further CSF-1 function in normal and, especially, in compromised pregnancy, we studied the pattern of its mRNA expression as well as expression of its receptor (c-fms) in the uteroplacental units of mice with induced (cyclophosphamide (CY)-treated) and spontaneous (CBA/J x DBA/2J mating combination) pregnancy loss. RNase protection analysis demonstrated the presence of two forms of CSF-1 mRNA in the uteroplacental unit corresponding to 1400- and 263-bp protective fragments. Densitometric analysis demonstrated that the level of 1400-bp mRNA form was decreased by 40% in the uteroplacental units of mice with CY-induced pregnancy loss compared with the control mice. About 20% decrease in 263-bp protective fragment was registered in resorbing versus non-resorbed placenta of CBA/J females mated to DBA/2J males. As judged by in situ hybridization assay, CSF-1 mRNA transcripts were localized in the uterine epithelium and stroma, while c-fms mRNA was found mainly in the trophoblast. The number of metrial gland cells as well as the number of uterine leucocytes expressing CSF-1 and c-fms mRNAs was substantially lower in the uteroplacental unit of mice with pregnancy loss than in control animals. Maternal immunostimulation, while significantly decreasing the resorption rate in mice with CY-induced pregnancy loss, also strengthened CSF-1 mRNA expression at the fetomaternal interface and resulted in reconstitution in the number of CSF-1+ uterine leucocytes and metrial gland cells. These data suggest a role for uterine CSF-1 in the physiology of normal and compromised pregnancy and demonstrate a possible involvement of CSF-1-associated signalling in mechanisms of placenta and endometrium repair following immunopotentiation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Abortion, Induced*
  • Abortion, Spontaneous / immunology*
  • Animals
  • Cyclophosphamide / pharmacology
  • Female
  • Gene Expression
  • Macrophage Colony-Stimulating Factor / biosynthesis*
  • Macrophage Colony-Stimulating Factor / genetics
  • Male
  • Mice
  • Mice, Inbred Strains
  • Placenta / immunology*
  • Placenta / pathology
  • Pregnancy
  • Rats
  • Rats, Long-Evans
  • Receptor, Macrophage Colony-Stimulating Factor / genetics
  • Uterus / immunology*
  • Uterus / pathology

Substances

  • Macrophage Colony-Stimulating Factor
  • Cyclophosphamide
  • Receptor, Macrophage Colony-Stimulating Factor