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Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage
Chronic enteritis can produce an excess of reactive oxygen species resulting in cellular damage. Stanniocalcin-1(STC-1) reportedly possesses anti-oxidative activity, the aim of this study was to define more clearly the direct contribution of STC-1 to anti-oxidative stress in cattle. In this study, p...
Autores principales: | , , , , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
The Korean Society of Veterinary Science
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269589/ https://www.ncbi.nlm.nih.gov/pubmed/24962416 http://dx.doi.org/10.4142/jvs.2014.15.4.475 |
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author | Wu, Li-ming Guo, Rui Hui, Lin Ye, Yong-gang Xiang, Jing-mei Wan, Chun-yun Zou, Miao Ma, Rui Sun, Xiao-zhuan Yang, Shi-jin Guo, Ding-zong |
author_facet | Wu, Li-ming Guo, Rui Hui, Lin Ye, Yong-gang Xiang, Jing-mei Wan, Chun-yun Zou, Miao Ma, Rui Sun, Xiao-zhuan Yang, Shi-jin Guo, Ding-zong |
author_sort | Wu, Li-ming |
collection | PubMed |
description | Chronic enteritis can produce an excess of reactive oxygen species resulting in cellular damage. Stanniocalcin-1(STC-1) reportedly possesses anti-oxidative activity, the aim of this study was to define more clearly the direct contribution of STC-1 to anti-oxidative stress in cattle. In this study, primary intestinal epithelial cells (IECs) were exposed to hydrogen peroxide (H(2)O(2)) for different time intervals to mimic chronic enteritis-induced cellular damage. Prior to treatment with 200 µM H(2)O(2), the cells were transfected with a recombinant plasmid for 48 h to over-express STC-1. Acridine orange/ethidium bromide (AO/EB) double staining and trypan blue exclusion assays were then performed to measure cell viability and apoptosis of the cells, respectively. The expression of STC-1 and apoptosis-related proteins in the cells was monitored by real-time PCR and Western blotting. The results indicated that both STC-1 mRNA and protein expression levels positively correlated with the duration of H(2)O(2) treatment. H(2)O(2) damaged the bovine IECs in a time-dependent manner, and this effect was attenuated by STC-1 over-expression. Furthermore, over-expression of STC-1 up-regulated Bcl-2 protein expression and slightly down-regulated caspase-3 production in the damaged cells. Findings from this study suggested that STC-1 plays a protective role in intestinal cells through an antioxidant mechanism. |
format | Online Article Text |
id | pubmed-4269589 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | The Korean Society of Veterinary Science |
record_format | MEDLINE/PubMed |
spelling | pubmed-42695892014-12-19 Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage Wu, Li-ming Guo, Rui Hui, Lin Ye, Yong-gang Xiang, Jing-mei Wan, Chun-yun Zou, Miao Ma, Rui Sun, Xiao-zhuan Yang, Shi-jin Guo, Ding-zong J Vet Sci Original Article Chronic enteritis can produce an excess of reactive oxygen species resulting in cellular damage. Stanniocalcin-1(STC-1) reportedly possesses anti-oxidative activity, the aim of this study was to define more clearly the direct contribution of STC-1 to anti-oxidative stress in cattle. In this study, primary intestinal epithelial cells (IECs) were exposed to hydrogen peroxide (H(2)O(2)) for different time intervals to mimic chronic enteritis-induced cellular damage. Prior to treatment with 200 µM H(2)O(2), the cells were transfected with a recombinant plasmid for 48 h to over-express STC-1. Acridine orange/ethidium bromide (AO/EB) double staining and trypan blue exclusion assays were then performed to measure cell viability and apoptosis of the cells, respectively. The expression of STC-1 and apoptosis-related proteins in the cells was monitored by real-time PCR and Western blotting. The results indicated that both STC-1 mRNA and protein expression levels positively correlated with the duration of H(2)O(2) treatment. H(2)O(2) damaged the bovine IECs in a time-dependent manner, and this effect was attenuated by STC-1 over-expression. Furthermore, over-expression of STC-1 up-regulated Bcl-2 protein expression and slightly down-regulated caspase-3 production in the damaged cells. Findings from this study suggested that STC-1 plays a protective role in intestinal cells through an antioxidant mechanism. The Korean Society of Veterinary Science 2014-12 2014-12-15 /pmc/articles/PMC4269589/ /pubmed/24962416 http://dx.doi.org/10.4142/jvs.2014.15.4.475 Text en © 2014 The Korean Society of Veterinary Science. http://creativecommons.org/licenses/by-nc/3.0/ This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/3.0/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Original Article Wu, Li-ming Guo, Rui Hui, Lin Ye, Yong-gang Xiang, Jing-mei Wan, Chun-yun Zou, Miao Ma, Rui Sun, Xiao-zhuan Yang, Shi-jin Guo, Ding-zong Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
title | Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
title_full | Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
title_fullStr | Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
title_full_unstemmed | Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
title_short | Stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
title_sort | stanniocalcin-1 protects bovine intestinal epithelial cells from oxidative stress-induced damage |
topic | Original Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4269589/ https://www.ncbi.nlm.nih.gov/pubmed/24962416 http://dx.doi.org/10.4142/jvs.2014.15.4.475 |
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