Mammary glands in male marsupials. 2. Development of teat primordia in Didelphis virginiana and Monodelphis domestica

1991 ◽  
Vol 3 (3) ◽  
pp. 295 ◽  
Author(s):  
ES Robinson ◽  
MB Renfree ◽  
RV Short ◽  
JL VandeBerg
Keyword(s):  
Mammary Gland ◽  
Mammary Gland Development ◽  
Mammary Glands ◽  
Monodelphis Domestica ◽  
Didelphis Virginiana ◽  
Adult Males ◽  
Young Males ◽  
Stage Of Development ◽  
Gland Development ◽  
Mammary Gland Expression

Young and adults of both sexes of two didelphid marsupials, Didelphis virginiana and Monodelphis domestica, were examined externally for evidence of mammary gland development. Female young possessed teat numbers typical of adult females (13-15 in D. virginiana; 11-13 in M. domestica). Male young showed variable teat numbers which were always low compared with females, with the majority possessing 2-4 in anterior positions. Teats were also present in adult males of both species, in similar numbers and locations to those of young males. There are no previous reports of the presence of teats in any adult male marsupials. No mammary primordia in males have been recorded at any stage of development in the most thoroughly studied Australian marsupials. Our findings strengthen the view that there is a dichotomy between the two marsupial lineages in the regulation of male mammary gland expression.

scholarly journals Progesterone Receptor Isoforms A and B: Temporal and Spatial Differences in Expression during Murine Mammary Gland Development

Endocrinology ◽  
2005 ◽  
Vol 146 (8) ◽  
pp. 3577-3588 ◽  
Author(s):  
Mark D. Aupperlee ◽  
Kyle T. Smith ◽  
Anastasia Kariagina ◽  
Sandra Z. Haslam
Keyword(s):  
Mammary Gland ◽  
Progesterone Receptor ◽  
Cyclin D1 ◽  
Mammary Gland Development ◽  
Minor Role ◽  
Normal Mammary Gland ◽  
Temporal Separation ◽  
Stage Of Development ◽  
Gland Development

Abstract Progesterone is a potent mitogen in the mammary gland. Based on studies using cells and animals engineered to express progesterone receptor (PR) isoforms A or B, PRA and PRB are believed to have different functions. Using an immunohistochemical approach with antibodies specific for PRA only or PRB only, we show that PRA and PRB expression in mammary epithelial cells is temporally and spatially separated during normal mammary gland development in the BALB/c mouse. In the virgin mammary gland when ductal development is active, the only PR protein isoform expressed was PRA. PRA levels were significantly lower during pregnancy, suggesting a minor role at this stage of development. PRB was abundantly expressed only during pregnancy, during alveologenesis. PRA and PRB colocalization occurred in only a small percentage of cells. During pregnancy there was extensive colocalization of PRB with 5-bromo-2′-deoxyuridine (BrdU) and cyclin D1; 95% of BrdU-positive cells and 83% of cyclin D1-positive cells expressed PRB. No colocalization of PRA with either BrdU or cyclin D1 was observed at pregnancy. In the virgin gland, PRA colocalization with BrdU or cyclin D1 was low; only 27% of BrdU-positive cells and 4% of cyclin D1-positive cells expressed PRA. The implication of these findings is that different actions of progesterone are mediated in PRB positive vs. PRA-positive cells in vivo. The spatial and temporal separation of PR isoform expression in mouse mammary gland provides a unique opportunity to determine the specific functions of PRA vs. PRB in vivo.

Progesterone receptor membrane component 1 is required for mammary gland development†

2020 ◽  
Vol 103 (6) ◽  
pp. 1249-1259
Author(s):  
Globinna Kim ◽  
Jong Geol Lee ◽  
Seung-A Cheong ◽  
Jung-Min Yon ◽  
Myeong Sup Lee ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Progesterone Receptor ◽  
Mammary Gland Development ◽  
Target Genes ◽  
Hormone Treatment ◽  
Mammary Glands ◽  
Membrane Component ◽  
Independent Manner ◽  
Receptor Membrane ◽  
Gland Development

Abstract The physiological functions of progesterone (P4) in female reproductive organs including the mammary glands are mediated via the progesterone receptor (PR), but not all P4 functions can be explained by PR-mediated signaling. Progesterone receptor membrane component 1 (PGRMC1), a potential mediator of P4 actions, plays an important role in the ovary and uterus in maintaining female fertility and pregnancy, but its function in mammary glands has not been elucidated. This study investigated the role of PGRMC1 in mouse mammary gland development. Unlike in the uterus, exogenous estrogen (E2) and/or P4 did not alter PGRMC1 expression in the mammary gland, and Pgrmc1-knockout (KO) mice displayed reduced ductal elongation and side branching in response to hormone treatment. During pregnancy, PGRMC1 was expressed within both the luminal and basal epithelium and gradually increased with gestation and decreased rapidly after parturition. Moreover, although lactogenic capacity was normal after parturition, Pgrmc1 KO resulted in defective mammary gland development from puberty until midpregnancy, while the expression of PR and its target genes was not significantly different between wild-type and Pgrmc1-KO mammary gland. These data suggest that PGRMC1 is essential for mammary gland development during puberty and pregnancy in a PR-independent manner.

scholarly journals Essential functions of p21-activated kinase 1 in morphogenesis and differentiation of mammary glands

2003 ◽  
Vol 161 (3) ◽  
pp. 583-592 ◽  
Author(s):  
Rui-An Wang ◽  
Ratna K. Vadlamudi ◽  
Rozita Bagheri-Yarmand ◽  
Iwan Beuvink ◽  
Nancy E. Hynes ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Gland Development ◽  
Mammary Epithelial Cells ◽  
Ectopic Expression ◽  
Functional Differentiation ◽  
Mammary Glands ◽  
Pregnancy And Lactation ◽  
P21 Activated Kinase ◽  
Gland Development

Although growth factors have been shown to influence mammary gland development, the nature of downstream effectors remains elusive. In this study, we show that the expression of p21-activated kinase (Pak)1, a serine/threonine protein kinase, is activated in mammary glands during pregnancy and lactation. By targeting an ectopic expression of a kinase-dead Pak1 mutant under the control of ovine β-lactoglobulin promoter, we found that the mammary glands of female mice expressing kinase-dead Pak1 transgene revealed incomplete lobuloalveolar development and impaired functional differentiation. The expression of whey acidic protein and β-casein and the amount of activated Stat5 in the nuclei of epithelial cells in transgenic mice were drastically reduced. Further analysis of the underlying mechanisms revealed that Pak1 stimulated β-casein promoter activity in normal mouse mammary epithelial cells and also cooperated with Stat5a. Pak1 directly interacted with and phosphorylated Stat5a at Ser 779, and both COOH-terminal deletion containing Ser 779 of Stat5a and the Ser 779 to Ala mutation completely prevented the ability of Pak1 to stimulate β-casein promoter. Mammary glands expressing inactive Pak1 exhibited a reduction of Stat5a Ser 779 phosphorylation. These findings suggest that Pak1 is required for alveolar morphogenesis and lactation function, and thus, identify novel functions of Pak1 in the mammary gland development.

scholarly journals Signal Transducer and Activator of Transcription 5a Mediates Mammary Ductal Branching and Proliferation in the Nulliparous Mouse

Endocrinology ◽  
2010 ◽  
Vol 151 (6) ◽  
pp. 2876-2885 ◽  
Author(s):  
Sarah J. Santos ◽  
Sandra Z. Haslam ◽  
Susan E. Conrad
Keyword(s):  
Mammary Gland ◽  
Epithelial Cells ◽  
Mammary Gland Development ◽  
Kinase Inhibitor ◽  
Mammary Epithelial Cells ◽  
Nuclear Factor Κb ◽  
Mammary Glands ◽  
Mammary Epithelial ◽  
Signal Transducer ◽  
Gland Development

Signal transducer and activator of transcription (Stat)5a is a critical regulator of mammary gland development. Previous studies have focused on Stat5a’s role in the late pregnant and lactating gland, and although active Stat5a is detectable in mammary epithelial cells in virgin mice, little is known about its role during early mammary gland development. In this report, we compare mammary gland morphology in pubertal and adult nulliparous wild-type and Stat5a−/− mice. The Stat5a-null mammary glands exhibited defects in secondary and side branching, providing evidence that Stat5a regulates these processes. In addition, Stat5a−/− mammary glands displayed an attenuated proliferative response to pregnancy levels of estrogen plus progesterone (E+P), suggesting that it plays an important role in early pregnancy. Finally, we examined one potential mediator of Stat5a’s effects, receptor activator of nuclear factor-κB ligand (RANKL). Stat5a−/− mammary glands were defective in inducing RANKL in response to E+P treatment. In addition, regulation of several reported RANKL targets, including inhibitor of DNA binding 2 (Id2), cyclin D1, and the cyclin-dependent kinase inhibitor p21Waf1/Cip1, was altered in Stat5a−/− mammary cells, suggesting that one or more of these proteins mediate the effects of Stat5a in E+P-treated mammary epithelial cells.

scholarly journals Abnormal Mammary Gland Development and Growth Retardation in Female Mice and MCF7 Breast Cancer Cells Lacking Androgen Receptor

2003 ◽  
Vol 198 (12) ◽  
pp. 1899-1908 ◽  
Author(s):  
Shuyuan Yeh ◽  
Yueh-Chiang Hu ◽  
Peng-Hui Wang ◽  
Chao Xie ◽  
Qingquan Xu ◽  
...  
Keyword(s):  
Breast Cancer ◽  
Mammary Gland ◽  
Androgen Receptor ◽  
Growth Factor ◽  
Growth Retardation ◽  
Breast Cancer Cells ◽  
Mammary Gland Development ◽  
Mammary Glands ◽  
Factor I ◽  
Gland Development

Phenotype analysis of female mice lacking androgen receptor (AR) deficient (AR−/−) indicates that the development of mammary glands is retarded with reduced ductal branching in the prepubertal stages, and fewer Cap cells in the terminal end buds, as well as decreased lobuloalveolar development in adult females, and fewer milk-producing alveoli in the lactating glands. The defective development of AR−/− mammary glands involves the defects of insulin-like growth factor I–insulin-like growth factor I receptor and mitogen-activated protein kinase (MAPK) signals as well as estrogen receptor (ER) activity. Similar growth retardation and defects in growth factor–mediated Ras/Raf/MAPK cascade and ER signaling are also found in AR−/− MCF7 breast cancer cells. The restoration assays show that AR NH2-terminal/DNA-binding domain, but not the ligand-binding domain, is essential for normal MAPK function in MCF7 cells, and an AR mutant (R608K), found in male breast cancer, is associated with the excessive activation of MAPK. Together, our data provide the first in vivo evidence showing that AR-mediated MAPK and ER activation may play important roles for mammary gland development and MCF7 breast cancer cell proliferation.

In Utero and Lactational Exposure to an Environmentally Relevant Mixture of Brominated Flame Retardants Induces a Premature Development of the Mammary Glands

2020 ◽  
Author(s):  
Rita-Josiane Gouesse ◽  
Elham Dianati ◽  
Alec McDermott ◽  
Michael G Wade ◽  
Barbara Hales ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Flame Retardants ◽  
Mammary Gland Development ◽  
Thyroid Hormone Receptor ◽  
Mammary Glands ◽  
Brominated Flame Retardants ◽  
In Utero ◽  
Proliferation Index ◽  
Lactational Exposure ◽  
Gland Development

Abstract In utero and prepubertal development of the mammary glands occurs minimally in a hormone independent manner until puberty where maturation of the hypothalamic-pituitary-gonadal axis drives an extensive remodeling. Nevertheless, because the immature glands contain functional hormone receptors, they are especially vulnerable to the effects of endocrine disruptors, such as brominated flame retardants (BFRs). BFRs are widespread chemicals added to household objects to reduce their flammability, and to which humans are ubiquitously exposed. We previously reported that in utero and lactational exposure to BFRs resulted in an impaired mammary gland development in peripubertal animals. Here, we assessed whether BFR-induced disruption of mammary gland development could manifest earlier in life. Dams were exposed prior to mating until pups’ weaning to a BFR mixture (0, 0.06, 20, or 60 mg/kg/day) formulated according to levels found in house dust. The mammary glands of female offspring were collected at weaning. Histo-morphological analyses showed that exposure to 0.06 mg/kg/day accelerates global epithelial development as demonstrated by a significant increase in total epithelial surface area, associated with a tendency to increase of the ductal area and thickness, and of lumen area. Significant increases of the Ki67 cell proliferation index and of the early apoptotic marker cleaved caspase-9 were also observed, as well as an upward trend in the number of thyroid hormone receptor α1 positive cells. These molecular, histologic, and morphometric changes are suggestive of accelerated pubertal development. Thus, our results suggest that exposure to an environmentally relevant mixture of BFRs induces precocious development of the mammary gland.

scholarly journals Gestational and Lactational Exposure to an Environmentally Relevant Mixture of Brominated Flame Retardants Downregulates Junctional Proteins, Thyroid Hormone Receptor α1 Expression, and the Proliferation-Apoptosis Balance in Mammary Glands Post Puberty

2019 ◽  
Vol 171 (1) ◽  
pp. 13-31 ◽  
Author(s):  
Rita-Josiane Gouesse ◽  
Mélanie Lavoie ◽  
Elham Dianati ◽  
Mike G Wade ◽  
Barbara F Hales ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Thyroid Hormone ◽  
Hormone Receptor ◽  
Flame Retardants ◽  
Mammary Gland Development ◽  
Thyroid Hormone Receptor ◽  
Mammary Glands ◽  
Lactational Exposure ◽  
Junctional Proteins ◽  
Gland Development

Abstract Mammary gland development requires hormonal regulation during puberty, pregnancy, and lactation. Brominated flame retardants (BFRs) are endocrine disruptors; they are added to consumer products to satisfy flammability standards. Previously, we showed that gestational and lactational exposure to an environmentally relevant mixture of BFRs disrupts proteins of the adherens junctions in rat dam mammary glands at weaning. Here, we hypothesize that perinatal exposure to the same BFR mixture also disrupts junctional proteins and signaling pathways controlling mammary gland development in pups. Dams were exposed through diet to a BFR mixture based on the substances in house dust; doses of the mixture used were 0, 0.06, 20, or 60 mg/kg/day. Dams were exposed continuously beginning prior to mating until pups’ weaning; female offspring were euthanized on postnatal day (PND) 21, 46, and 208. The lowest dose of BFRs significantly downregulated adherens junction proteins, E-cadherin, and β-catenin, and the gap junction protein p-Cx43, as well as thyroid hormone receptor alpha 1 protein at PND 46. No effects were observed on estrogen or progesterone receptors. The low dose also resulted in a decrease in cleaved caspase-3, a downward trend in PARP levels, proteins involved in apoptosis, and an upward trend in proliferating cell nuclear antigen, a marker of proliferation. No effects were observed on ductal elongation or on the numbers of terminal end buds. Together, our results indicate that gestational and lactational exposure to an environmentally relevant mixture of BFRs disrupts cell-cell interactions, thyroid hormone homeostasis and the proliferation-apoptosis balance at PND 46, a critical stage for mammary gland development.

Mammary gland development of sows injected with growth hormone-releasing factor during gestation and(or) lactation

1997 ◽  
Vol 77 (2) ◽  
pp. 335-338 ◽  
Author(s):  
C. Farmer ◽  
G. Pelletier ◽  
P. Brazeau ◽  
D. Petitclerc
Keyword(s):  
Growth Hormone ◽  
Mammary Gland ◽  
Key Words ◽  
Mammary Gland Development ◽  
Mammary Glands ◽  
Late Gestation ◽  
Chemical Analyses ◽  
Growth Hormone Releasing Factor ◽  
Mammary Cell ◽  
Gland Development

Twenty-four gilts received s.c. injections of saline or growth hormone-releasing factor (GRF) in late gestation and(or) lactation. Sows were sacrificed on day 30 of lactation and functional mammary glands were excised for chemical analyses. Weight of parenchymal (P = 0.004) and extra-parenchymal tissues (P = 0.002) were decreased with GRF injections during lactation. Parenchymal mass per milligram of DNA also decreased (P = 0.025) with GRF in lactation while parenchymal DNA concentration increased (P = 0.03). Exogenous GRF given to sows during lactation therefore decreased total parenchymal mass, increased cell density and decreased mammary cell size. Key words: Sow, mammary gland, growth hormone-releasing factor

THE SECRETORY CAPACITY OF THE AUTOTRANSPLANTED HYPOPHYSIS AS INDICATED BY THE EFFECTS OF STEROID HORMONES ON THE MAMMARY GLANDS

1961 ◽  
Vol 38 (3) ◽  
pp. 449-468 ◽  
Author(s):  
Kurt Ahrén
Keyword(s):  
Growth Hormone ◽  
Mammary Gland ◽  
Pituitary Gland ◽  
Mammary Gland Development ◽  
Mammary Glands ◽  
Male Rats ◽  
Alveolar Development ◽  
Hypophysectomized Rats ◽  
Gland Development ◽  
Secretory Capacity

ABSTRACT In the present experiments the secretory capacity of the pituitary gland, autotransplanted to the kidney capsule, was studied with special regard to the secretion of prolactin and growth hormone, using the response of the mammary glands to oestrone (3-hydroxy-oestra-1,3,5(10)-trien-17-one) and progesterone (pregn-4-ene-3,20-dione) in castrated female and male rats as indicator. The main results were as follows: 1) Daily injections of 10 μg of oestrone + 4 mg of progesterone stimulated slight duct growth and marked but not maximal lobule-alveolar development in the mammary glands of rats with transplanted hypophysis. In rats with intact pituitary gland this treatment produced more extensive duct growth and more marked alveolar development. 2) Daily injections of 1 μg of oestrone did not stimulate mammary gland development in rats with transplanted pituitary gland. The same treatment produced slight but definite duct growth in rats with intact pituitary gland. 3) Daily injections of 10 μg of oestrone stimulated slight duct growth and restricted lobule-alveolar development in rats with transplanted hypophysis. In rats with intact pituitary gland this treatment produced more extensive growth of the duct system. 4) In hypophysectomized rats all dose levels of oestrone and progesterone were ineffective in promoting mammary gland development. Combined with prolactin these hormones stimulated, in hypophysectomized rats, a mammary gland development which, qualitatively as well as quantitatively, was very similar to that found in rats with transplanted pituitary gland. These results indicate that the transplanted pituitary gland secreted considerable amounts of prolactin but did not secrete growth hormone or secreted it in only very small amounts.

scholarly journals Role of F-Box Protein βTrcp1 in Mammary Gland Development and Tumorigenesis

2004 ◽  
Vol 24 (18) ◽  
pp. 8184-8194 ◽  
Author(s):  
Yasusei Kudo ◽  
Daniele Guardavaccaro ◽  
Patricia G. Santamaria ◽  
Ryo Koyama-Nasu ◽  
Esther Latres ◽  
...  
Keyword(s):  
Mammary Gland ◽  
Transgenic Mice ◽  
Mammary Gland Development ◽  
Mammary Glands ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Ductal Branching ◽  
F Box Protein ◽  
Gland Development

ABSTRACT The F-box protein βTrcp1 controls the stability of several crucial regulators of proliferation and apoptosis, including certain inhibitors of the NF-κB family of transcription factors. Here we show that mammary glands of βTrcp1−/− female mice display a hypoplastic phenotype, whereas no effects on cell proliferation are observed in other somatic cells. To investigate further the role of βTrcp1 in mammary gland development, we generated transgenic mice expressing human βTrcp1 targeted to epithelial cells under the control of the mouse mammary tumor virus (MMTV) long terminal repeat promoter. Compared to controls, MMTV βTrcp1 mammary glands display an increase in lateral ductal branching and extensive arrays of alveolus-like protuberances. The mammary epithelia of MMTV βTrcp1 mice proliferate more and show increased NF-κB DNA binding activity and higher levels of nuclear NF-κB p65/RelA. In addition, 38% of transgenic mice develop tumors, including mammary, ovarian, and uterine carcinomas. The targeting of βTrcp1 to lymphoid organs produces no effects on these tissues. In summary, our results support the notion that βTrcp1 positively controls the proliferation of breast epithelium and indicate that alteration of βTrcp1 function and expression may contribute to malignant behavior of breast tumors, at least in part through NF-κB transactivation.

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