The Regulation of the Prolactin Receptor Gene Expression in the Mammary Gland of Early Pregnant Mouse.

Mizoguchi, Yasushi; Kim, Jae Young; Enami, Jumpei; Sakai, Senkiti

doi:10.1507/endocrj.44.53

Cited by 27 publications

(12 citation statements)

References 27 publications

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“…In the mammary glands of mice ovariectomized during early pregnancy, both E 2 and PRL upregulate PRLR-LF mRNA expression, while it is suppressed by P (Mizoguchi et al 1997). PRL upregulates PRLR levels in the mammary glands of pseudopregnant rabbits, while P prevents this PRL-induced upregulation (Djiane & Durand 1977).…”

Section: Discussionmentioning

confidence: 94%

Tissue-specific regulation of porcine prolactin receptor expression by estrogen, progesterone, and prolactin

Trott

Horigan

Gloviczki

et al. 2009

Journal of Endocrinology

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Prolactin (PRL) acts through its receptor (PRLR) via both endocrine and local paracrine/autocrine pathways to regulate biological processes including reproduction and lactation. We analyzed the tissue-and stage of gestationspecific regulation of PRL and PRLR expression in various tissues of pigs. Abundance of pPRLR-long form (LF) mRNA increased in the mammary gland and endometrium during gestation while in other tissues it remained constant. There was a parallel increase in the abundance of the pPRLR-LF protein in the mammary gland and endometrium during gestation. We determined the hormonal regulation of pPRLR-LF mRNA expression in various tissues from ovariectomized, hypoprolactinemic gilts given combinations of the replacement hormones estrogen (E 2 ), progestin (P), and/or haloperidol-induced PRL. Abundance of pPRLR-LF mRNA in kidney and liver was unaffected by hormone treatments. Expression of uterine pPRLR-LF mRNA was induced by E 2 whereas the effect of E 2 was abolished by co-administering P. The expression of pPRLR-LF mRNA in the mammary gland stroma was induced by PRL, whereas E 2 induced its expression in the epithelium. In contrast to these changes in pPRLR expression, pPRL expression was relatively constant and low during gestation in all tissues except the pituitary. Taken together, these data reveal that specific combinations of E 2 , P, and PRL differentially regulate pPRLR-LF expression in the endometrium and mammary glands, and that the action of PRL on its target tissues is dependent upon pPRLR-LF abundance more so than the local PRL expression.

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Section: Discussionmentioning

confidence: 94%

Tissue-specific regulation of porcine prolactin receptor expression by estrogen, progesterone, and prolactin

Trott

Horigan

Gloviczki

et al. 2009

Journal of Endocrinology

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“…PRL, on the other hand, has been demonstrated to increase estrogen receptor expression in mammary epithelial cells in vitro (7). The estrogen receptor is known to increase both progesterone receptor (PR) and PRL-R expression (11,28). PR signaling is indispensable for the formation of small side branches in terminal duct lobular units and alveologenesis (3,16).…”

Section: Discussionmentioning

confidence: 99%

Impaired Alveologenesis and Maintenance of Secretory Mammary Epithelial Cells in Jak2 Conditional Knockout Mice

Wagner

Krempler

Triplett

et al. 2004

Molecular and Cellular Biology

147

129

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Jak2 is a hormone-receptor-coupled kinase that mediates the tyrosine phosphorylation and activation of signal transducers and activators of transcription (Stat). The biological relevance of Jak2-Stat signaling in hormone-responsive adult tissues is difficult to investigate since Jak2 deficiency leads to embryonic lethality. We generated Jak2 conditional knockout mice to study essential functions of Jak2 during mammary gland development. The mouse mammary tumor virus-Cre-mediated excision of the first coding exon resulted in a Jak2 null mutation that uncouples signaling from the prolactin receptor (PRL-R) to its downstream mediator Stat5 in the presence of normal and supraphysiological levels of PRL. Jak2-deficient females were unable to lactate as a result of impaired alveologenesis. Unlike Stat5a knockouts, multiple gestation cycles could not reverse the Jak2-deficient phenotype, suggesting that neither other components of the PRL-R signaling cascade nor other growth factors and their signal transducers were able to compensate for the loss of Jak2 function to activate Stat5 in vivo. A comparative analysis of Jak2-deficient mammary glands with transplants from Stat5a/b knockouts revealed that Jak2 deficiency also impairs the pregnancy-induced branching morphogenesis. Jak2 conditional mutants therefore resemble PRL-R knockouts more closely, which suggested that Jak2 deficiency might affect additional PRL-R downstream mediators other than Stat5a and Stat5b. To address whether Jak2 is required for the maintenance of PRL-responsive, differentiating alveolar cells, we utilized a transgenic strain that expresses Cre recombinase under regulatory elements of the whey acidic protein gene (Wap). The Wap-Cre-mediated excision of Jak2 resulted in a negative selection of differentiated alveolar cells, suggesting that Jak2 is required not only for the proliferation and differentiation of alveolar cells but also for their maintenance during lactation.

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“…Previous studies have reported that E2 can increase prolactin receptor expression in both mice and humans in cells outside the immune system [29][30][31]. Results from Figure 2 show that E2 treatment increases prolactin receptor expression in cells of the immune system as well, as both B and CD4 T cells showed significant increases.…”

Section: Discussionmentioning

confidence: 74%

Diminished prolactin from chlordecone treatment in ovariectomized (NZB×NZW)F1 mice

Wang¹,

Roberts²,

Butfiloski³

et al. 2007

International Immunopharmacology

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In murine models of systemic lupus erythematosus (SLE), administration of either prolactin or estradiol (E2) increases autoimmunity, and there is evidence that elevated prolactin in response to E2 administration may contribute substantially to E2 effects. Hormonal influence on SLE can extend to environmental agents, as demonstrated by the ability of estrogenic organochlorine pesticides such as chlordecone to accelerate the development of lupus in female (NZB x NZW)F 1 mice. In order to evaluate a potential role for prolactin in chlordecone effects on SLE, it was necessary to first determine whether treatment with chlordecone, like E2, results in elevated prolactin levels. Ovariectomized (NZB x NZW)F 1 mice were treated for 5-6 weeks with chlordecone or E2 in doses shown previously to significantly shorten the time to onset of SLE. At the end of the treatment period, serum prolactin levels were increased 10-to 20-fold in E2-treated mice compared to untreated controls, but decreased in an apparent dose-dependent manner in mice treated with chlordecone. Prolactin receptor in purified B and CD4 T cells from treated animals, assessed through measurement of mRNA using quantitative real-time PCR, was increased by E2 treatment but unchanged in response to chlordecone. These observations suggest that the role of prolactin in eliciting autoimmunity in E2-treated animals is absent in the case of chlordecone, and by implication, that chlordecone possesses other actions that can replace the contribution of prolactin to development of SLE.

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The Regulation of the Prolactin Receptor Gene Expression in the Mammary Gland of Early Pregnant Mouse.

Cited by 27 publications

References 27 publications

Tissue-specific regulation of porcine prolactin receptor expression by estrogen, progesterone, and prolactin

Tissue-specific regulation of porcine prolactin receptor expression by estrogen, progesterone, and prolactin

Impaired Alveologenesis and Maintenance of Secretory Mammary Epithelial Cells in Jak2 Conditional Knockout Mice

Diminished prolactin from chlordecone treatment in ovariectomized (NZB×NZW)F1 mice

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