ROLE OF RECEPTORS FOR EPIDERMAL GROWTH-FACTOR AND INSULIN-LIKE GROWTH-FACTOR-I AND GROWTH-FACTOR-II IN THE DIFFERENTIATION OF RAT MAMMARY-GLANDS FROM LACTOGENESIS-I TO LACTOGENESIS-II

Citation
Le. Bussmann et al., ROLE OF RECEPTORS FOR EPIDERMAL GROWTH-FACTOR AND INSULIN-LIKE GROWTH-FACTOR-I AND GROWTH-FACTOR-II IN THE DIFFERENTIATION OF RAT MAMMARY-GLANDS FROM LACTOGENESIS-I TO LACTOGENESIS-II, Journal of Reproduction and Fertility, 107(2), 1996, pp. 307-314
Citations number
48
Categorie Soggetti
Reproductive Biology
ISSN journal
00224251
Volume
107
Issue
2
Year of publication
1996
Pages
307 - 314
Database
ISI
SICI code
0022-4251(1996)107:2<307:RORFEG>2.0.ZU;2-2
Abstract
In addition to ovarian steroids and lactogenic hormones from the place nta and pituitary, growth factors control the growth and differentiati on of mammary glands. Lactogenesis II at the end of pregnancy is under the control of progesterone. Ovariectomy results in a significant dec rease in the number of receptors for epidermal growth factor (EGF) and insulin-like growth factor I (IGF-I) and an increase in IGF-II bindin g sites in mammary gland acini of rats, without affecting the affinity for their respective ligand. Although concentrations of EGF, IGF-I an d IGF-II receptors are regulated by oestradiol and progesterone, repla cement treatment with ovarian steroids after ovariectomy showed that r eceptor concentrations do not mediate the restraint on lactogenesis. P rogesterone treatment; which inhibits the onset of lactogenesis II, di d not restore EGF receptor concentrations to control values, and the p resence of oestradiol was required to reverse the effect of ovariectom y. Oestradiol, which potentiates the effect of ovariectomy on milk syn thesis, increases IGF-I receptor concentrations. IGF-II receptor conce ntrations, after the different steroid treatments, were consistent wit h the steroid effect on milk synthesis. The changes observed in the co ncentrations of these growth factor receptors at the onset of mammary gland secretion are not considered to affect the progesterone block to lactogenesis II, but rather are a consequence of the shift of the hor monal and, hence, physiological status of the gland.