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Prolactin and glucocorticoid signaling induces lactation-specific tight junctions concurrent with beta-casein expression in mammary epithelial cells

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Biochim. Biophys. Acta, Mol. Cell Res. 1863-8_2006-2016.pdf2.51 MBPDFView/Open
Please use this identifier to cite or link to this item:http://hdl.handle.net/2115/65154

Title: Prolactin and glucocorticoid signaling induces lactation-specific tight junctions concurrent with beta-casein expression in mammary epithelial cells
Authors: Kobayashi, Ken Browse this author →KAKEN DB
Tsugami, Yusaku Browse this author
Matsunaga, Kota Browse this author
Oyama, Shoko Browse this author
Kuki, Chinatsu Browse this author
Kumura, Haruto Browse this author →KAKEN DB
Keywords: Glucocorticoid
Tight junction
Mammary gland
Epithelial cellProlactin
Issue Date: Aug-2016
Publisher: Elsevier
Journal Title: Biochimica et Biophysica Acta (BBA) Molecular Cell Research
Volume: 1863
Issue: 8
Start Page: 2006
End Page: 2016
Publisher DOI: 10.1016/j.bbamcr.2016.04.023
PMID: 27130254
Abstract: Alveolar mammary epithelial cells (MECs) in mammary glands are highly specialized cells that produce milk for suckling infants. Alveolar MECs also form less permeable tight junctions (TJs) to prevent the leakage of milk components after parturition. In the formation process of less permeable TJs, MECs show a selective downregulation of Cldn4 and a localization change of Cldn3. To investigate what induces less permeable TJs through these compositional changes in Cldns, we focused on two lactogenesis-related hormones: prolactin (Prl) and glucocorticoids. Prl caused a downregulation of Cldn3 and Cldn4 with the formation of leaky TJs in MECs in vitro. Prl-treated MECs also showed low beta-casein expression with the activation of STAT5 signaling. By contrast, dexamethasone (Dex), a glucocorticoid analogue, upregulated Cldn3 and Cldn4, concurrent with the formation of less permeable TJs and the activation of glucocorticoid signaling without the expression of beta-casein. Cotreatment with Prl and Dex induced the selective downregulation of Cldn4 and the concentration of Cldn3 in the region of Tjs concurrent with less permeable TJ formation and high beta-casein expression. The inhibition of Prl secretion by bromocriptine in lactating mice induced the upregulation of Cldn3 and Cldn4 concurrent with the downregulation of milk production. These results indicate that the coactivation of Prl and glucocorticoid signaling induces lactation-specific less permeable TJs concurrent with lactogenesis.
Rights: ©2016, Elsevier. This manuscript version is made available under the CC-BY-NC-ND 4.0 license http://creativecommons.org/licenses/by-nc-nd/4.0/
http://creativecommons.org/licenses/by-nc-nd/4.0/
Type: article (author version)
URI: http://hdl.handle.net/2115/65154
Appears in Collections:農学院・農学研究院 (Graduate School of Agriculture / Faculty of Agriculture) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 小林 謙

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