title: Colony-stimulating factor-1 (CSF-1) expression in the uteroplacental unit of mice with spontaneous and induced pregnancy loss.
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.
authors.affiliation: Department of Embryology and Teratology, Sackler School of Medicine, Tel Aviv University, Tel Aviv, Israel.
authors.forename: M
authors.initials: M
authors.lastname: Gorivodsky
authors.forename: A
authors.initials: A
authors.lastname: Torchinsky
authors.forename: J
authors.initials: J
authors.lastname: Shepshelovich
authors.forename: S
authors.initials: S
authors.lastname: Savion
authors.forename: A
authors.initials: A
authors.lastname: Fein
authors.forename: H
authors.initials: H
authors.lastname: Carp
authors.forename: V
authors.initials: V
authors.lastname: Toder
mesh_terms: D000028:Abortion, Induced; D000022:Abortion, Spontaneous / Q000276:immunology*; D000818:Animals; D003520:Cyclophosphamide / Q000494:pharmacology; D005260:Female; D015870:Gene Expression; D016173:Macrophage Colony-Stimulating Factor / Q000096:biosynthesis* / Q000235:genetics; D008297:Male; D051379:Mice; D008815:Mice, Inbred Strains; D010920:Placenta / Q000276:immunology* / Q000473:pathology; D011247:Pregnancy; D051381:Rats; D020318:Rats, Long-Evans; D016186:Receptor, Macrophage Colony-Stimulating Factor / Q000235:genetics; D014599:Uterus / Q000276:immunology* / Q000473:pathology
chemical_list: D016173:Macrophage Colony-Stimulating Factor; D003520:Cyclophosphamide; D016186:Receptor, Macrophage Colony-Stimulating Factor