FIBROBLAST GROWTH-FACTOR-1 AND GROWTH-FACTOR-2 IN THE PRIMATE UTERUS

Citation
Ca. Samathanam et al., FIBROBLAST GROWTH-FACTOR-1 AND GROWTH-FACTOR-2 IN THE PRIMATE UTERUS, Biology of reproduction, 59(3), 1998, pp. 491-496
Citations number
18
Categorie Soggetti
Reproductive Biology
Journal title
ISSN journal
00063363
Volume
59
Issue
3
Year of publication
1998
Pages
491 - 496
Database
ISI
SICI code
0006-3363(1998)59:3<491:FGAGIT>2.0.ZU;2-1
Abstract
Fibroblast growth factors (FGF) 1 and 2 are paracrine effecters of pro liferation and angiogenesis in many tissues. To elucidate potential ro les for these growth factors in uterine plasticity, we used in situ hy bridization histochemistry to identify the cellular sources of FGF-1 a nd -2 production, and immunohistochemistry to identify the cellular an d extracellular deposition sites of the peptides in the primate uterus . To evaluate the effects of estradiol on uterine FGFs, uteri from ova riectomized rhesus monkeys treated with estradiol- or vehicle-containi ng pellets were investigated. FGF-1 and -2 mRNAs were both expressed i n uterine epithelial and myometrial cells. Quantitative comparison of their mRNA levels using computerized grain counting showed no signific ant difference between estradiol- and vehicle-treated animals. FGF-1 i mmunoreactivity was detected in scattered epithelial, vascular, and my ometrial cells in the vehicle-treated animals but found to be signific antly more intense and widespread in estradiol-treated animals. In bot h conditions, FGF-1 immunostaining was predominantly nuclear. FGF-2 im munoreactivity was concentrated extracellularly in the basal lamina of both glandular and surface epithelium and was abundant and diffusely distributed within myometrial and vascular cells in both cytoplasm and nucleus. There was no apparent difference in the pattern or intensity of FGF-2 immunostaining related to estradiol treatment. These data de monstrate that major uterine cell types synthesize both FGF-1 and -2, and that the two peptides are differentially localized in uterine cell ular and extracellular compartments and differentially sensitive to re gulation by estradiol.