scholarly journals Polyamine transport and metabolism in mouse mammary gland. General properties and hormonal regulation.

1976 ◽  
Vol 251 (9) ◽  
pp. 2795-2800
Author(s):  
K Kano ◽  
T Oka
Keyword(s):  
Mammary Gland ◽  
Hormonal Regulation ◽  
Mouse Mammary Gland ◽  
General Properties ◽  
Polyamine Transport

HORMONAL REGULATION OF RNA AND PROTEIN SYNTHESIS IN THE MOUSE MAMMARY GLAND BEFORE AND DURING LACTATION

1971 ◽  
Vol 50 (2) ◽  
pp. 281-291 ◽  
Author(s):  
M. R. BANERJEE ◽  
FERNE M. ROGERS ◽  
D. N. BANERJEE
Keyword(s):  
Protein Synthesis ◽  
Mammary Gland ◽  
Hormonal Regulation ◽  
Rna Synthesis ◽  
Mouse Mammary Gland ◽  
Synthetic Activity ◽  
Tissue Homogenate ◽  
Mammary Tissue ◽  
Leucine Incorporation

SUMMARY As measured by [3H]uridine incorporation in vivo, the low rate of RNA synthesis in the mammary gland of virgin C3H and BALB/c mice increased sixfold in the mammary tissue of 15-day pregnant mice. In the 5-day lactating gland, RNA synthesis was ten times higher than that in virgin mammary tissue. On the 10th day of lactation this increased RNA synthetic activity in the mammary gland was considerably reduced but was still twice that of the mammary tissue of virgin mice. Twenty-four hours after adrenalectomy, RNA synthesis in lactating glands was reduced by over 80%, whereas in the mammary gland before lactation, it was reduced by 20–30% only. A single i.p. injection of 250 μg of cortisol led to a threefold increase of RNA synthesis within 1 to 2 h in lactating glands of adrenalectomized mice; this was followed by a decline. Incorporation of [3H]leucine into trichloroacetic acid-insoluble material from lactating mammary tissue was used as a measure of'total protein' synthesis, and [3H]leucine radioactivity determined in Ca2+−rennin precipitate of 105000 g supernatant of lactating mammary tissue homogenate was used as a measure of casein synthesis. Adrenalectomy caused a 50% reduction of 'total protein' synthesis, whereas synthesis of 'casein-like' phosphoprotein virtually stopped after the operation. The injection of cortisol into adrenalectomized mice induced a selective increase of [3H]leucine incorporation into the casein of lactating glands. The results indicate that RNA synthesis in the mammary tissue is more dependent on adrenal hormones during the functional than the structural state of differentiation. The hormonal regulation of RNA synthesis and its role in milk protein synthesis in the mammary gland in vivo is discussed.

scholarly journals Differential Hormonal Regulation and Function of Progesterone Receptor Isoforms in Normal Adult Mouse Mammary Gland

Endocrinology ◽  
2007 ◽  
Vol 148 (5) ◽  
pp. 2290-2300 ◽  
Author(s):  
Mark D. Aupperlee ◽  
Sandra Z. Haslam
Keyword(s):  
Mammary Gland ◽  
Hormonal Regulation ◽  
Adult Mouse ◽  
Mouse Mammary Gland ◽  
Functional Roles ◽  
Progesterone Receptor Isoforms ◽  
Receptor Isoforms ◽  
Mitogenic Action ◽  
And Function

In normal mouse mammary gland, the mitogenic action of progesterone (P) is mediated by two P receptor (PR) isoforms, PRA and PRB. PRA is predominantly expressed in the adult virgin, and PRB is predominantly expressed during pregnancy. To investigate hormonal regulation of PR isoform expression and isoform-specific functions in vivo, adult ovariectomized BALB/c mice were treated for 3, 5, or 10 d with estrogen (E), P, or estrogen plus progesterone (E+P). Using an immunohistochemical approach with isoform-specific antibodies, we investigated hormonal regulation of PRA and PRB and their functional roles in proliferation and morphogenesis. Significant E-induced proliferation was only observed after 5 d at the distal tips of ducts; there was no sidebranching or alveologenesis. P induced proliferation that resulted in sidebranching and alveologenesis, but E+P treatment produced more proliferation sooner and more extensive sidebranching and alveologenesis. PRA levels were increased by E and decreased by P. Increased PRB levels were induced by treatment with P or E+P and coincided with the formation of alveoli. PRA was the predominant PR isoform expressed during sidebranching, and colocalization of PRA with 5-bromo-2′-deoxyuridine revealed that proliferation of PRA-positive and -negative cells was responsible for P-induced sidebranching. PRB was the predominant PR isoform expressed during alveologenesis, and colocalization of PRB with 5-bromo-2′-deoxyuridine showed that both PRB-positive and -negative cells proliferated during alveolar expansion. These results demonstrate different hormonal regulation of PRA and PRB levels in vivo and suggest that P can induce proliferation through either PRA or PRB via direct and paracrine mechanisms.

scholarly journals Metabolism of the chemopreventive retinoid N-(4-hydroxyphenyl)retinamide by mammary gland in organ culture

1988 ◽  
Vol 256 (2) ◽  
pp. 579-584 ◽  
Author(s):  
R G Mehta ◽  
T A Hultin ◽  
R C Moon
Keyword(s):  
Mammary Gland ◽  
Organ Culture ◽  
Steroid Hormones ◽  
Hormonal Regulation ◽  
Mammary Carcinogenesis ◽  
Reversed Phase ◽  
Mouse Mammary Gland ◽  
Mammary Cells ◽  
Chemically Induced ◽  
Chloroform Methanol

N-(4-Hydroxyphenyl)retinamide (4-HPR) is considered to be the most effective chemopreventive retinoid for chemically induced mammary carcinogenesis in rats. However, the mechanism of 4-HPR action in mammary cells is poorly understood. In the present study we examined the metabolism of 4-HPR in the mouse mammary gland in organ culture. Mammary glands excised from BALB/c mice were incubated with 4-HPR in the presence of insulin, prolactin and steroid hormones for 6 days. The glands were extracted with chloroform/methanol (2:1, v/v), and the metabolites were separated on a reversed-phase h.p.l.c. column. Three metabolites were separated in addition to 4-HPR; one of the metabolites, M2, was co-eluted with 13-cis-4-HPR, M3 was co-eluted with N-(4-methoxyphenyl)retinamide (4-MPR) and M1 remains unidentified. There appeared to be some hormonal regulation in the distribution of metabolites in the glands. Increased levels of 4-MPR and M1 were observed in insulin-plus-prolactin-treated glands as compared with the glands incubated with steroid hormones. Furthermore, it was observed that M1 isolated from the livers of 4-HPR-treated rats competed for the cellular retinoic acid-binding protein (CRABP) sites; however, 4-HPR did not bind to CRABP. These results indicate that mouse mammary gland can metabolize 4-HPR and that the metabolites which compete for CRABP sites may have physiological significance in the retinoid inhibition of mammary carcinogenesis.

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