Mammary Gland Development

Ormandy, Christopher J.; Horseman, Nelson D.; Naylor, Matthew J.; Harris, Jessica; Robertson, Fiona G.; Binart, Nadine; Kelly, Paul A.

doi:10.1007/978-1-4615-1683-5_11

Cited by 9 publications

(9 citation statements)

References 41 publications

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“…It is also known that, in cycling females, prolactin (PRL) is only indirectly involved in the formation of ductal side branching by promoting luteal progesterone synthesis, as evident by the restoration of ductal branching in PRL knockout females treated with progesterone [19,20]. In accordance with these references, we did not detected PRL receptor (PRLR) expression in membrane of ductal epithelium of cycling vizcachas (Figure 3).…”

Section: Cyclingsupporting

confidence: 86%

Ovarian, Hypophyseal and Hypothalamic Hormones Coordinate Mammary Gland Remodeling in Adult Lagostomus maximus: a Rodent that Shows Pseudo-Ovulation at Mid-Gestation

Halperín¹,

Dorfman²,

Vitullo³

2017

Current Topics in Lactation

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Adult female mammary glands go through extensive tissue remodeling during pregnancy, lactation and after the weaning of the neonates. Here we characterize mammary gland morphology of adult females of Lagostomus maximus, a hystricomorph rodent with a pseudo-ovulatory event at mid-gestation, and describe how the glandular tissue changes its architecture in response to variations of the hormonal environment. At mid-gestation, pseudo-ovulation is seen as an essential event increasing the number of secondary corpora lutea and thus rising the circulating levels of progesterone that help to maintain pregnancy to term. As a side effect, mammary gland development is favored early during the long-lasting pregnancy of L. maximus, preparing females for the nutritional need of fully developed pups in this k-strategist species.

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Section: Cyclingsupporting

confidence: 86%

Ovarian, Hypophyseal and Hypothalamic Hormones Coordinate Mammary Gland Remodeling in Adult Lagostomus maximus: a Rodent that Shows Pseudo-Ovulation at Mid-Gestation

Halperín¹,

Dorfman²,

Vitullo³

2017

Current Topics in Lactation

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“…Despite the ability of both Stat5 and Stat3 to promote processes linked to carcinogenesis (reviewed in Bromberg, 2002;Buettner et al, 2002), these related transcription factors exert opposing activities on alveolar development and invasion, in addition to the distinct effects on AP-1 activity reported here (reviewed in Ormandy et al, 2001;Watson, 2001;Hennighausen and Robinson, 2005;Sultan et al, 2005). Interestingly, Stat3 correlated with Stat5 expression in the limited number of mammary cell lines examined herein, and higher expression was associated with reduced AP-1 responses to PRL, not the increase predicted from the actions of Stat3 alone.…”

Section: Stat5 Inhibits Prl Activation Of Ap-1 Jh Gutzman Et Almentioning

confidence: 82%

“…Stat5, particularly Stat5a, mediates most of the actions of PRL in alveologenesis (reviewed in Ormandy et al, 2001;Hennighausen and Robinson, 2005). PRLactivated Jak2 rapidly phosphorylates Stat5 on Tyr 694 (Tyr 699 in a highly conserved position in Stat5b, and among different species) resulting in dimerization, translocation to the nucleus, and subsequent participation in transcriptional regulation (reviewed in Shemanko and Groner, 2001;Goffin et al, 2005).…”

Section: Introductionmentioning

confidence: 99%

Stat5 activation inhibits prolactin-induced AP-1 activity: distinct prolactin-initiated signals in tumorigenesis dependent on cell context

et al. 2007

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The essential role of prolactin (PRL) in normal mammary gland growth and differentiation has implicated this hormone in the development and progression of breast cancer. Although Stat5 is the best-characterized mediator of PRL signals, PRL also activates multiple other signals, whose roles in normal and pathologic processes are not well understood. We have shown that PRL stimulates activating protein-1 (AP-1) activity in breast cancer cells, and can cooperate with estradiol in this pathway. AP-1 modulates many processes critical for carcinogenesis, including cell proliferation, survival, transformation, invasion and angiogenesis, and is elevated in many neoplasms, including breast tumors. Here, we investigated the relationship between PRL signals to AP-1 and Stat5. We found that PRL activation of Stat5a and Stat5b, but not Stat1 or Stat3, reduced PRL signals to AP-1, without altering estradiol-induced AP-1 activity. The truncation mutant, Stat5/D53C, but not Stat5Y699F, was an effective inhibitor, consistent with a requirement for Stat5 dimerization and nuclear accumulation, but not its C-terminal transactivation activity. The association of Stat5 with AP-1 proteins suggests that this underlies the inhibition. Predictably, the ability of PRL to activate Stat5 and AP-1 was inversely related in mammary cell lines. Further, reduction of Stat5 protein with siRNA in T47D cells, which contain elevated Stat5, increased PRLinduced AP-1 signals, transcripts for the AP-1 target, matrix metalloproteinase-2 and associated invasive behavior. This study points to the importance of cell context in determining the spectrum of PRL-induced actions, which is critical for understanding the contributions of PRL to breast cancer.

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“…As noted, Hedgehog, Wnt10b, and PTHrP drive embryonic development, after which estrogen, growth hormone, and IGF1 are essential for growth of the dichotomous ductal tree. Progesterone (P4), PRL, or PL induce the growth and differentiation of lobuloalveoli (16)(17)(18)(19). These lobuloalveoli, or lobules, are the primary functional units of mammary gland secretion, and important details of their development have been learned over the past few years.…”

Section: Development Of the Mammary Glandsmentioning

confidence: 99%

Serotonin: A Local Regulator in the Mammary Gland Epithelium

Horseman

Collier

2014

Annu. Rev. Anim. Biosci.

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Serotonin (5-hydroxytryptamine, 5-HT) is a very simple molecule that plays key roles in complex communication mechanisms within the animal body. In the mammary glands, serotonin biosynthesis and secretion are induced in response to dilation of the alveolar spaces. Since its discovery several years ago, mammary 5-HT has been demonstrated to perform two homeostatic functions. First, serotonin regulates lactation and initiates the transition into the earliest phases of involution. Second, serotonin is a local signal that induces parathyroid hormone-related peptide (PTHrP), which allows the mammary gland to drive the mobilization of calcium from the skeleton. These processes use different receptor types, 5-HT7 and 5-HT2, respectively. In this review, we provide synthetic perspectives on the fundamental processes of lactation homeostasis and the adaptation of calcium homeostasis for lactation. We analyze the role of the intrinsic serotonin system in the physiological regulation of the mammary glands. We also consider the importance of the mammary serotonin system in pathologies and therapies associated with lactation and breast cancer.

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Mammary Gland Development

Cited by 9 publications

References 41 publications

Ovarian, Hypophyseal and Hypothalamic Hormones Coordinate Mammary Gland Remodeling in Adult Lagostomus maximus: a Rodent that Shows Pseudo-Ovulation at Mid-Gestation

Ovarian, Hypophyseal and Hypothalamic Hormones Coordinate Mammary Gland Remodeling in Adult Lagostomus maximus: a Rodent that Shows Pseudo-Ovulation at Mid-Gestation

Stat5 activation inhibits prolactin-induced AP-1 activity: distinct prolactin-initiated signals in tumorigenesis dependent on cell context

Serotonin: A Local Regulator in the Mammary Gland Epithelium

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