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.

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 Loss of glutaredoxin 3 impedes mammary lobuloalveolar development during pregnancy and lactation

2017 ◽  
Vol 312 (3) ◽  
pp. E136-E149 ◽  
Author(s):  
Khanh Pham ◽  
Jie Dong ◽  
Xiqian Jiang ◽  
Ying Qu ◽  
Han Yu ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Mammary Gland Development ◽  
Redox Homeostasis ◽  
Physiological Role ◽  
Cell Types ◽  
Normal Mammary Gland ◽  
Pregnancy And Lactation ◽  
Gland Development ◽  
Lobuloalveolar Development

Mammalian glutaredoxin 3 (Grx3) has been shown to be important for regulating cellular redox homeostasis in the cell. Our previous studies indicate that Grx3 is significantly overexpressed in various human cancers including breast cancer and demonstrate that Grx3 controls cancer cell growth and invasion by regulating reactive oxygen species (ROS) and NF-κB signaling pathways. However, it remains to be determined whether Grx3 is required for normal mammary gland development and how it contributes to epithelial cell proliferation and differentiation in vivo. In the present study, we examined Grx3 expression in different cell types within the developing mouse mammary gland (MG) and found enhanced expression of Grx3 at pregnancy and lactation stages. To assess the physiological role of Grx3 in MG, we generated the mutant mice in which Grx3 was deleted specifically in mammary epithelial cells (MECs). Although the reduction of Grx3 expression had only minimal effects on mammary ductal development in virgin mice, it did reduce alveolar density during pregnancy and lactation. The impairment of lobuloalveolar development was associated with high levels of ROS accumulation and reduced expression of milk protein genes. In addition, proliferative gene expression was significantly suppressed with proliferation defects occurring in knockout MECs during alveolar development compared with wild-type controls. Therefore, our findings suggest that Grx3 is a key regulator of ROS in vivo and is involved in pregnancy-dependent mammary gland development and secretory activation through modulating cellular ROS.

scholarly journals Progesterone Receptor Isoforms and Proliferation in the Rat Mammary Gland during Development

Endocrinology ◽  
2007 ◽  
Vol 148 (6) ◽  
pp. 2723-2736 ◽  
Author(s):  
Anastasia Kariagina ◽  
Mark D. Aupperlee ◽  
Sandra Z. Haslam
Keyword(s):  
Mammary Gland ◽  
Progesterone Receptor ◽  
Mammary Gland Development ◽  
Kinase Inhibitors ◽  
Expression Patterns ◽  
Significant Proportion ◽  
Myoepithelial Cells ◽  
Normal Mammary Gland ◽  
Rat Mammary Gland ◽  
Gland Development

Progesterone (P), acting through progesterone receptor (PR) isoforms A and B, plays an important role in normal mammary gland development and is implicated in the etiology of breast cancer. Because of significant similarities between human and rat mammary gland development and hormonal responsiveness of mammary cancers, we investigated P action in the rat mammary gland. By immunohistochemical methods we determined PRA and PRB expression at puberty, sexual maturity, pregnancy, and lactation and after postlactational involution and their functional roles in the regulation of proliferation. PRA expression was restricted to luminal epithelial cells, whereas PRB was expressed in both luminal and myoepithelial cells, indicating a novel role of PRB in myoepithelial cell regulation. The majority of PRA-positive (PRA+) cells coexpressed PRB. In the pubertal and adult virgin mammary gland, PRA+PRB+ cells also expressed nuclear cyclin D1 but did not contain the proliferation marker bromodeoxyuridine. Based on a lack of phosphorylated retinoblastoma protein expression and the expression patterns of the cyclin-dependent kinase inhibitors p21 and p27 in these cells, we conclude that PRA+PRB+ cells appear to be cell cycle arrested and do not proliferate. PRA+ cells were decreased in the adult gland and during and after pregnancy. The percentage of PRB+ cells was relatively constant throughout development, and in a significant proportion of cells, only PRB was detected. During development, and especially during pregnancy, a high percentage of PRB+ cells were positive for bromodeoxyuridine. From this observation, we conclude that these cells proliferate and that P acting through PRB may directly stimulate proliferation.

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