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
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
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.