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SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro
Suppressor of cytokine signaling 3 (SOCS3) is a cytokine-induced negative feedback-loop regulator of cytokine signaling. More and more evidence has proved it to be an inhibitor of signal transducers and activators of transcription 5 (STAT5). Here, we used dairy cow mammary epithelial cells (DCMECs)...
Autores principales: | , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
MDPI
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6270101/ https://www.ncbi.nlm.nih.gov/pubmed/24141248 http://dx.doi.org/10.3390/molecules181012987 |
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author | Huang, Yu-Ling Zhao, Feng Luo, Chao-Chao Zhang, Xia Si, Yu Sun, Zhe Zhang, Li Li, Qing-Zhang Gao, Xue-Jun |
author_facet | Huang, Yu-Ling Zhao, Feng Luo, Chao-Chao Zhang, Xia Si, Yu Sun, Zhe Zhang, Li Li, Qing-Zhang Gao, Xue-Jun |
author_sort | Huang, Yu-Ling |
collection | PubMed |
description | Suppressor of cytokine signaling 3 (SOCS3) is a cytokine-induced negative feedback-loop regulator of cytokine signaling. More and more evidence has proved it to be an inhibitor of signal transducers and activators of transcription 5 (STAT5). Here, we used dairy cow mammary epithelial cells (DCMECs) to analyze the function of SOCS3 and the interaction between SOCS3 and STAT5a. The expression of SOCS3 was found in cytoplasm and nucleus of DCMECs by fluorescent immunostaining. Overexpression and inhibition of SOCS3 brought a remarkable milk protein synthesis change through the regulation of JAK2/STAT5a pathway activity, and SOCS3 expression also decreased SREBP-1c expression and fatty acid synthesis. Inhibited STAT5a activation correlated with reduced SOCS3 expression, which indicated that SOCS3 gene might be one of the targets of STAT5a activation, DCMECs treated with L-methionine (Met) resulted in a decrease of SOCS3 expression. SOCS3 could also decrease cell proliferation and viability by CASY-TT detection. Together, our findings indicate that SOCS3 acts as an inhibitor of JAK2/STAT5a pathway and disturbs fatty acid synthesis by decreasing SREBP-1c expression, which validates its involvement in both milk protein synthesis and fat synthesis. In aggregate, these results reveal that low SOCS3 expression is required for milk synthesis and proliferation of DCMECs in vitro. |
format | Online Article Text |
id | pubmed-6270101 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | MDPI |
record_format | MEDLINE/PubMed |
spelling | pubmed-62701012018-12-18 SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro Huang, Yu-Ling Zhao, Feng Luo, Chao-Chao Zhang, Xia Si, Yu Sun, Zhe Zhang, Li Li, Qing-Zhang Gao, Xue-Jun Molecules Article Suppressor of cytokine signaling 3 (SOCS3) is a cytokine-induced negative feedback-loop regulator of cytokine signaling. More and more evidence has proved it to be an inhibitor of signal transducers and activators of transcription 5 (STAT5). Here, we used dairy cow mammary epithelial cells (DCMECs) to analyze the function of SOCS3 and the interaction between SOCS3 and STAT5a. The expression of SOCS3 was found in cytoplasm and nucleus of DCMECs by fluorescent immunostaining. Overexpression and inhibition of SOCS3 brought a remarkable milk protein synthesis change through the regulation of JAK2/STAT5a pathway activity, and SOCS3 expression also decreased SREBP-1c expression and fatty acid synthesis. Inhibited STAT5a activation correlated with reduced SOCS3 expression, which indicated that SOCS3 gene might be one of the targets of STAT5a activation, DCMECs treated with L-methionine (Met) resulted in a decrease of SOCS3 expression. SOCS3 could also decrease cell proliferation and viability by CASY-TT detection. Together, our findings indicate that SOCS3 acts as an inhibitor of JAK2/STAT5a pathway and disturbs fatty acid synthesis by decreasing SREBP-1c expression, which validates its involvement in both milk protein synthesis and fat synthesis. In aggregate, these results reveal that low SOCS3 expression is required for milk synthesis and proliferation of DCMECs in vitro. MDPI 2013-10-17 /pmc/articles/PMC6270101/ /pubmed/24141248 http://dx.doi.org/10.3390/molecules181012987 Text en © 2013 by the authors; licensee MDPI, Basel, Switzerland. http://creativecommons.org/licenses/by/3.0/ This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution license (http://creativecommons.org/licenses/by/3.0/). |
spellingShingle | Article Huang, Yu-Ling Zhao, Feng Luo, Chao-Chao Zhang, Xia Si, Yu Sun, Zhe Zhang, Li Li, Qing-Zhang Gao, Xue-Jun SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro |
title | SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro |
title_full | SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro |
title_fullStr | SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro |
title_full_unstemmed | SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro |
title_short | SOCS3-Mediated Blockade Reveals Major Contribution of JAK2/STAT5 Signaling Pathway to Lactation and Proliferation of Dairy Cow Mammary Epithelial Cells in Vitro |
title_sort | socs3-mediated blockade reveals major contribution of jak2/stat5 signaling pathway to lactation and proliferation of dairy cow mammary epithelial cells in vitro |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6270101/ https://www.ncbi.nlm.nih.gov/pubmed/24141248 http://dx.doi.org/10.3390/molecules181012987 |
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