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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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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)
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Submitter: 小林 謙
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