Rat mammary gland nuclear RNA polymerases in late pregnancy and lactation

1973 ◽  
Vol 299 (4) ◽  
pp. 576-587 ◽  
Author(s):  
I.S. Mendelson ◽  
K.M. Anderson
Keyword(s):  
Mammary Gland ◽  
Late Pregnancy ◽  
Rna Polymerases ◽  
Nuclear Rna ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland

scholarly journals Expression of Prolactin mRNA in Rat Mammary Gland During Pregnancy and Lactation

2000 ◽  
Vol 48 (3) ◽  
pp. 389-395 ◽  
Author(s):  
Toshiki Iwasaka ◽  
Shinobu Umemura ◽  
Kochi Kakimoto ◽  
Haruko Koizumi ◽  
Yoshiyuki R. Osamura
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Epithelial Cells ◽  
Late Pregnancy ◽  
Mammary Epithelial ◽  
Rt Pcr ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Pcr Method

We studied the expression of prolactin (PRL) mRNA in the mammary gland of resting, pregnant, lactating, and weanling rats using in situ and solution reverse transcriptase-polymerase chain reaction (RT-PCR). In mid- to late pregnancy and throughout lactation, PRL mRNA was detected in both in situ and solution RT-PCR. These PRL mRNA signals were clearly identified in the cytoplasm of alveolar and ductal mammary epithelial cells by the in situ RT-PCR method. In mid- to late pregnancy, such as at the initiating point of PRL mRNA expression, we confirmed in some cases a lack of PRL mRNA by solution RT-PCR. In addition, in the early weaning phase, no signals were detected by solution RT-PCR. However, slight focal signals were detected in some poorly vacuolated cytoplasm of regressing acinar cells by in situ RT-PCR. These findings suggest that PRL mRNA in rat mammary gland begins in mid- to late pregnancy in parallel with the development of the mammary gland, continues throughout lactation, and declines in the early phase of weaning, with regression of mammary epithelial cells.

Mammary gland function and development: effect of zinc deficiency in rat

1980 ◽  
Vol 238 (1) ◽  
pp. E26-E31 ◽  
Author(s):  
P. B. Mutch ◽  
L. S. Hurley
Keyword(s):  
Mammary Gland ◽  
Zinc Deficiency ◽  
Dna Content ◽  
Late Pregnancy ◽  
Female Rats ◽  
Deficient Diet ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Gland Function ◽  
Zinc Deficient Diet

The effect of dietary zinc deficiency during late pregnancy and lactation on the rat mammary gland was investigated by feeding female rats either a zinc-deficient diet (0.4 ppm Zn) or a zinc-sufficient diet (100 ppm Zn) ad libitum or restricted in amount. Zinc deficiency from day 0 of lactation specifically reduced the total RNA content of lactating mammary glands on day 14, but had no effect beyond that of food restriction on their total DNA content, Both RNA and DNA content of the mammary gland were decreased by reduced food intake. Zinc deficiency from day 14 of pregnancy to day 2 of lactation severely impaired parturition and prevented the normal rise in mammary gland RNA seen during lactogenesis in control animals. A shorter deficiency period, from day 18 of gestation, had no effect on mammary gland nucleic acids other than that due to inanition.

scholarly journals Polyamine biogenesis in the rat mammary gland during pregnancy and lactation

1972 ◽  
Vol 130 (1) ◽  
pp. 71-76 ◽  
Author(s):  
Diane H. Russell ◽  
Thomas A. McVicker
Keyword(s):  
Mammary Gland ◽  
Late Pregnancy ◽  
Normal Mammary Gland ◽  
Biosynthetic Activity ◽  
A Value ◽  
Lactating Mammary Gland ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Gland Development ◽  
Very High

Polyamines and RNA accumulate in the rat mammary gland during pregnancy, but the major increases occur after parturition. Therefore the major increases occur after the gland has obtained its maximal complement of epithelial cells. During lactation, the spermidine concentration rises above 5mm and RNA content in the lactating mammary gland reaches a value 16 times that of the unstimulated mammary gland. The ratio of spermidine/spermine, an increase of which initially signals an elevation in biosynthetic activity, is near 1 in the normal mammary gland and is greater than 10 in the lactating mammary gland. Putrescine concentration is very low during the entire course of mammary-gland development, with the exception of early pregnancy. The low putrescine concentration probably reflects the very rapid conversion of putrescine into spermidine. Both ornithine decarboxylase, the enzyme that synthesizes putrescine, and putrescine-stimulated S-adenosyl-l-methionine decarboxylase, the enzyme that synthesizes spermidine, increase in activity during middle and late pregnancy; during lactation, both enzyme activities are elevated until the 21st day of lactation, and then decline. These declines are concomitant with involution. Also, it was found that the amount of ribonuclease activity in the mammary gland was very high during lactation, almost double that in the gland during pregnancy.

β-Adrenergic Receptors in the Rat Mammary Gland during Pregnancy and Lactation: Characterization, Distribution, and Coupling to Adenylate Cyclase

Endocrinology ◽  
1990 ◽  
Vol 126 (1) ◽  
pp. 565-574 ◽  
Author(s):  
BIANCA MARCHETTI ◽  
MICHEL-A FORTIER ◽  
PATRICK POYET ◽  
NICOLLE FOLLEA ◽  
GEORGES PELLETIER ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Adenylate Cyclase ◽  
Adrenergic Receptors ◽  
Pregnancy And Lactation ◽  
Rat Mammary Gland ◽  
Β Adrenergic Receptors

Mammary gland cell content during various phases of lactation

1962 ◽  
Vol 203 (5) ◽  
pp. 939-941 ◽  
Author(s):  
Richard C. Moon
Keyword(s):  
Mammary Gland ◽  
Deoxyribonucleic Acid ◽  
Cellular Proliferation ◽  
Gland Cell ◽  
Late Pregnancy ◽  
Mammary Glands ◽  
Lactation Period ◽  
Cell Content ◽  
Rat Mammary Gland ◽  
Mammary Gland Cell

Deoxyribonucleic acid (DNA) was used as an index of the cellular state of the rat mammary gland in late pregnancy ( day 20) and early ( day 1), intense ( day 14), and declining ( day 28) lactation. Dams sacrificed on day 28 of lactation were provided with foster litters on day 14 postpartum to insure a strong sucking stimulus during the lactation period from days 14–28. Mammary DNA increased 57% from day 20 of pregnancy to lactation day 14, but no significant change in DNA content was evident by day 1 of lactation. A significantly lower DNA concentration was observed in mammary glands of rats sacrificed at lactation day 28 when compared with that of animals killed at day 14 of lactation. The data suggest that cellular proliferation of mammary gland continues well into lactation and that a decline in lactation may be due, in part, to a reduction in the number of milk-secreting cells.

scholarly journals Has the mammary gland a protective mechanism against overexposure to triiodothyronine during the peripartum period? The prolactin pulse down-regulates mammary type I deiodinase responsiveness to norepinephrine

2004 ◽  
Vol 183 (2) ◽  
pp. 267-277 ◽  
Author(s):  
B Anguiano ◽  
R Rojas-Huidobro ◽  
G Delgado ◽  
C Aceves
Keyword(s):  
Mammary Gland ◽  
Critical Role ◽  
Alveolar Epithelium ◽  
Late Pregnancy ◽  
Protective Mechanism ◽  
Type I ◽  
Key Factor ◽  
Pregnancy And Lactation ◽  
Contrary Effect ◽  
Peripartum Period

Peripartum is a crucial period for mammary gland final differentiation and the onset of lactation. Although the ‘trigger’ for lactogenesis depends on several hormones, a key factor is the peripartum prolactin (PRL) pulse whose deletion results in a failure to initiate milk production. Other hormones having a critical role during this period but exerting a contrary effect are the thyronines. A transitory hypothyroidism occurs at peripartum in serum and several other extrathyroidal tissues, whereas the induction of hyperthyroidism during late pregnancy is associated with the absence of lactation after delivery. We analyzed the mammary gland during pregnancy and lactation for: (a) the type and amount of thyroid receptors (TRs), (b) the local triiodothyronine (T3) generation catalyzed by type I deiodinase (Dio1), (c) the Dio1 response to norepinephrine (NE) and (d) the effect on Dio1 and TRs of blocking the PRL pulse at peripartum. Our data showed that during pregnancy the mammary gland contains Dio1 in low amounts associated with the highest expression of TRα1; whereas during lactation the gland shows high levels of both Dio1 and TRα1. However, at peripartum, both TRs and Dio1 decrease, and Dio1 becomes refractory to NE. This refractoriness disappears when the PRL pulse is blocked by the dopamine agonist bromocriptine. This blockade is also accompanied by a significant decrease in cyclin D1 expression. Our data suggested that the peripartum PRL pulse is part of a protective mechanism against precocious differentiation and/or premature involution of the alveolar epithelium due to T3 overexposure.

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