Mammary Fat Can Adjust Prolactin Effect on Mammary Epithelial Cells via Leptin and Estrogen

Feuermann, Yonatan; Mabjeesh, S.J.; Shamay, Avi

doi:10.1155/2009/427260

Cited by 27 publications

(22 citation statements)

References 37 publications

(49 reference statements)

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“…Adipocytes secrete numerous factors that can impact mammary gland function, such as leptin and estrogen (73). The persistence of these factors may have adverse consequences on lactation.…”

Section: Discussionmentioning

confidence: 99%

Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation

Lee

Hennigar

Alam

et al. 2015

Journal of Biological Chemistry

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Background: ZnT2 is expressed in non-secreting and secreting mammary epithelium; however, the physiological role is not understood. Results: ZnT2-null mice have impaired mammary expansion and compromised mammary differentiation and milk secretion during lactation. Conclusion: ZnT2-mediated zinc transport is critical for mammary development and function during lactation. Significance: This study identifies novel consequences of ZnT2 function in the mammary gland.

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“…Adipocytes secrete numerous factors that can impact mammary gland function, such as leptin and estrogen (73). The persistence of these factors may have adverse consequences on lactation.…”

Section: Discussionmentioning

confidence: 99%

Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation

Lee

Hennigar

Alam

et al. 2015

Journal of Biological Chemistry

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“…On the contrary, Garofalo et al [2004] showed that leptin alone had no significant effects on ERα expression in the cytoplasmic and nuclear compartments in MCF‐7 cells. Feuermann et al [2009] found that leptin upregulated the expression of ERα in the mammary epithelial cells in a dose‐dependent manner. These findings supported our hypothesis that leptin regulated the expression of ERs in ATDC5 cells.…”

Section: Discussionmentioning

confidence: 99%

Leptin regulates estrogen receptor gene expression in ATDC5 cells through the extracellular signal regulated kinase signaling pathway

Wang

Jiang

et al. 2012

J of Cellular Biochemistry

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Both estrogen and leptin play an important role in the regulation of physiological processes of endochondral bone formation in linear growth. Estrogen receptors (ERα and ERβ) are known as members of the superfamily of nuclear steroid hormone receptors and are detected in all zones of growth plate chondrocytes. They can be regulated in a ligand-independent manner. Whether leptin regulates ERs in the growth plate is still not clear. To explore this issue, chondrogenic ATDC5 cells were used in the present study. Messenger RNA and protein analyses were performed by quantitative PCR and Western blotting. We found that both ERα and ERβ were dynamically expressed during the ATDC5 cell differentiation for 21 days. Leptin (50 ng/ml) significantly upregulated ERα and ERβ mRNA and protein levels 48 h after leptin stimulation (P<0.05) at day 14. The up-regulation of ERα and ERβ mRNA by leptin was shown in a dose-dependent manner, but the most effective dose of leptin was different (100 and 1,000 ng/ml, respectively). Furthermore, we confirmed that leptin augmented the phosphorylation of ERK1/2 in a time-dependent manner. A maximum eightfold change was observed at 15 min. Finally, a specific ERK1/2 inhibitor, UO126, blocked leptin-induced ERs regulation in ATDC5 cells, indicating that ERK1/2 mediates, partly, the effects of leptin on ERs. These data demonstrate, for the first time, that leptin regulates the expression of ERs in growth plate chondrocytes via ERK signaling pathway, thereby suggesting a crosstalk between leptin and estrogen receptors in the regulation of bone formation.

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“…In fact, immunosuppressed animals may have a higher concentration of PRL, since this hormone stimulates the physiology of immune cells; this mechanism, however, is still uncertain and needs further studies [18,19].…”

Section: Discussionmentioning

confidence: 99%

The progesterone and estrogen modify the uterine prolactin and prolactin receptor expression of hyperprolactinemic mice

Amaral

Carvalho

Maciel

et al. 2014

Gynecological Endocrinology

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The aim of this study was to evaluate the effects of metoclopramide-induced hyperprolactinemia on the prolactin (PRL) and PRL receptor's expression in the uterus of mice. For this purpose, 49 Swiss mice were divided into the following groups: GrSS (non-ovariectomized mice given vehicle); GrMET (non-ovariectomized mice treated with metoclopramide); OvSS (ovariectomized mice given vehicle); OvMET (ovariectomized mice treated with metoclopramide); OvMET+17βE (ovariectomized mice treated with metoclopramide and 17β estradiol); OvMET+MP (ovariectomized mice treated with metoclopramide and micronized progesterone); OvMET+17βE+MP (ovariectomized mice treated with metoclopramide and a solution of 17β estradiol and micronized progesterone). Immunohistochemical analyzes were evaluated semi-quantitatively. Our results showed that GrMET, OvMET+MP, and OvMET+17βE+MP presented strong PRL expression. OvMET and OvMET+17βE presented mild reaction, while GrSS and OvSS presented weak reaction. Concerning PRL receptor, OvMET+MP and OvMET+17βE+MP showed strong reaction; GrMET, OvSS, and OvMET+17βE showed mild reaction; and GrSS and OvMET showed weak reaction. These findings suggest that progesterone alone or in combination with estrogen may increase the expression of uterine PRL and PRL receptor.

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Mammary Fat Can Adjust Prolactin Effect on Mammary Epithelial Cells via Leptin and Estrogen

Cited by 27 publications

References 37 publications

Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation

Essential Role for Zinc Transporter 2 (ZnT2)-mediated Zinc Transport in Mammary Gland Development and Function during Lactation

Leptin regulates estrogen receptor gene expression in ATDC5 cells through the extracellular signal regulated kinase signaling pathway

The progesterone and estrogen modify the uterine prolactin and prolactin receptor expression of hyperprolactinemic mice

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