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SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis
Acute obstructive cholangitis (AOC) is a common and severe infectious diseases that occurs in an obstructed biliary system. The suppressors of cytokine signaling (SOCS) family include well-known negative regulators of cytokine receptor signaling. However, few studies have been conducted to determine...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Nature Publishing Group UK
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573403/ https://www.ncbi.nlm.nih.gov/pubmed/28842621 http://dx.doi.org/10.1038/s41598-017-09865-z |
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author | Yu, Jianhua Zhang, Weiguang Qian, Hongwei Tang, Haijun Lin, Weiguo Lu, Baochun |
author_facet | Yu, Jianhua Zhang, Weiguang Qian, Hongwei Tang, Haijun Lin, Weiguo Lu, Baochun |
author_sort | Yu, Jianhua |
collection | PubMed |
description | Acute obstructive cholangitis (AOC) is a common and severe infectious diseases that occurs in an obstructed biliary system. The suppressors of cytokine signaling (SOCS) family include well-known negative regulators of cytokine receptor signaling. However, few studies have been conducted to determine their function in AOC. In this study, we showed that SOCS1 expression aberrantly changed and was associated with AOC prognosis in rat models. Decreased SOCS1 expression enhances regenerative response after biliary drainage (BD) resulting from AOC by upregulating hepatocyte growth factor (HGF) signaling. To detect SOCS1 expression in the liver less invasively and to predict the prognosis for AOC after BD, miR-221 and miR-222 were investigated. Ectopic SOCS1 expression indirectly decreases miR-221/222 expression through Met in vitro. An inverse correlation between SOCS1 expression and miR-221/222 expression in liver tissue or in serum was verified in rats. Serum from AOC patients showed that lower expression of circulating miR-221/222 after endoscopic nasobiliary drainage was associated with delayed restoration of liver function. Our results showed that SOCS1 regulates hepatic regenerative response, and indirectly detecting downstream molecules, such as miR-221/222, may provide prognostic makers for AOC. |
format | Online Article Text |
id | pubmed-5573403 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Nature Publishing Group UK |
record_format | MEDLINE/PubMed |
spelling | pubmed-55734032017-09-01 SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis Yu, Jianhua Zhang, Weiguang Qian, Hongwei Tang, Haijun Lin, Weiguo Lu, Baochun Sci Rep Article Acute obstructive cholangitis (AOC) is a common and severe infectious diseases that occurs in an obstructed biliary system. The suppressors of cytokine signaling (SOCS) family include well-known negative regulators of cytokine receptor signaling. However, few studies have been conducted to determine their function in AOC. In this study, we showed that SOCS1 expression aberrantly changed and was associated with AOC prognosis in rat models. Decreased SOCS1 expression enhances regenerative response after biliary drainage (BD) resulting from AOC by upregulating hepatocyte growth factor (HGF) signaling. To detect SOCS1 expression in the liver less invasively and to predict the prognosis for AOC after BD, miR-221 and miR-222 were investigated. Ectopic SOCS1 expression indirectly decreases miR-221/222 expression through Met in vitro. An inverse correlation between SOCS1 expression and miR-221/222 expression in liver tissue or in serum was verified in rats. Serum from AOC patients showed that lower expression of circulating miR-221/222 after endoscopic nasobiliary drainage was associated with delayed restoration of liver function. Our results showed that SOCS1 regulates hepatic regenerative response, and indirectly detecting downstream molecules, such as miR-221/222, may provide prognostic makers for AOC. Nature Publishing Group UK 2017-08-25 /pmc/articles/PMC5573403/ /pubmed/28842621 http://dx.doi.org/10.1038/s41598-017-09865-z Text en © The Author(s) 2017 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/. |
spellingShingle | Article Yu, Jianhua Zhang, Weiguang Qian, Hongwei Tang, Haijun Lin, Weiguo Lu, Baochun SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
title | SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
title_full | SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
title_fullStr | SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
title_full_unstemmed | SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
title_short | SOCS1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
title_sort | socs1 regulates hepatic regenerative response and provides prognostic makers for acute obstructive cholangitis |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5573403/ https://www.ncbi.nlm.nih.gov/pubmed/28842621 http://dx.doi.org/10.1038/s41598-017-09865-z |
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