Developmental and hormonal regulated gene expression of fibroblast growth factor 2 (FGF-2) and its receptors in porcine endometrium

This study examined the mRNA levels of the fibroblast growth factor 2 (FGF-2) and two of its receptors, FGFR1IIIc and FGFR2IIIc, at days 12 and 20 of the ovarian cycle (DC 12 and DC 20), days 1 and 12 of pregnancy (DP 1 and DP 12) as well as the influence of progesterone (P) and estradiolbenzoate (EB) on their expression in the. endometrium of ovariectomized (ovx) gilts by real-time PCR. Proteins of FGF-2 and FGFR1 were immunolocalized. FGF-2 and FGFR2IIIc mRNAs were always found with a 5- to 30-fold higher absolute concentration compared to FGFR1IIIc. The latter transcript significantly declined between DP 1 and DP 12, whereas FGF-2 and FGFR2IIIc showed no significant changes at that time. FGF-2 transcription was greater at DC 20 than at DC 12, but significantly most transcripts were found in ovx gilts. EB induced a significant suppression of FGF-2 mRNA, an effect which was antagonized by P and even prevented by P + EB. FGFR1IIIc mRNA was significantly increased at DC 20, that of FGFR2IIIc at DC 12 displaying a 10 times higher absolute mRNA amount. Suppression of FGFR1IIIc mRNA by P was abolished by EB while P + EB attenuated this effect. FGFR2IIIc transcripts were equally restrained by P or EB while a combination of both slightly reduced such declines. Localization of FGF-2 and FGFR I proteins in stromal, glandular and vascular compartments was effected by sex steroids. Both proteins were strongly expressed at DP 12 but not at DP 1. Summarized, differential temporal and spatial localization of FGF-2 and FGFR 1 after response to sex steroids support a complex regulation of this ligand receptor system important for proliferation and differentiation of uterine cells including angiogenic processes. While FGFR1IIIc is presumed to be promoted by estradiol FGFR2IIIc appears to be dominated by progesterone implicating different biological importance for a functional endometrium. (C) 2004 Elsevier Ltd. All rights reserved.