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Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells
Infection of Helicobacter pylori (H. pylori) changed the proliferation of gastric epithelial cells and decreased the expression of heat shock protein 70 (HSP70). However, the effects of H. pylori on the proliferation of gastric epithelial cells and the roles of HSP70 during the progress need further...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Hindawi Publishing Corporation
2014
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4138794/ https://www.ncbi.nlm.nih.gov/pubmed/25161665 http://dx.doi.org/10.1155/2014/794342 |
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author | Tao, Liping Zou, Hai Huang, Zhimin |
author_facet | Tao, Liping Zou, Hai Huang, Zhimin |
author_sort | Tao, Liping |
collection | PubMed |
description | Infection of Helicobacter pylori (H. pylori) changed the proliferation of gastric epithelial cells and decreased the expression of heat shock protein 70 (HSP70). However, the effects of H. pylori on the proliferation of gastric epithelial cells and the roles of HSP70 during the progress need further investigation. Objective. To investigate the effects of Helicobacter pylori (H. pylori) and heat shock protein 70 (HSP70) on the proliferation of human gastric epithelial cells. Methods. H. pylori and a human gastric epithelial cell line (AGS) were cocultured. The proliferation of AGS cells was quantitated by an MTT assay, and the expression of HSP70 in AGS cells was detected by Western blotting. HSP70 expression in AGS cells was silenced by small interfering RNA (siRNA) to investigate the role of HSP70. The siRNA-treated AGS cells were cocultured with H. pylori and cell proliferation was measured by an MTT assay. Results. The proliferation of AGS cells was accelerated by coculturing with H. pylori for 4 and 8 h, but was suppressed at 24 and 48 h. HSP70 expression was decreased in AGS cells infected by H. pylori for 48 h. The proliferation in HSP70-silenced AGS cells was inhibited after coculturing with H. pylori for 24 and 48 h compared with the control group. Conclusions. Coculture of H. pylori altered the proliferation of gastric epithelial cells and decreased HSP70 expression. HSP70 knockdown supplemented the inhibitory effect of H. pylori on proliferation of epithelial cells. These results indicate that the effects of H. pylori on the proliferation of gastric epithelial cells at least partially depend on the decreased expression of HSP70 induced by the bacterium. |
format | Online Article Text |
id | pubmed-4138794 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2014 |
publisher | Hindawi Publishing Corporation |
record_format | MEDLINE/PubMed |
spelling | pubmed-41387942014-08-26 Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells Tao, Liping Zou, Hai Huang, Zhimin Gastroenterol Res Pract Research Article Infection of Helicobacter pylori (H. pylori) changed the proliferation of gastric epithelial cells and decreased the expression of heat shock protein 70 (HSP70). However, the effects of H. pylori on the proliferation of gastric epithelial cells and the roles of HSP70 during the progress need further investigation. Objective. To investigate the effects of Helicobacter pylori (H. pylori) and heat shock protein 70 (HSP70) on the proliferation of human gastric epithelial cells. Methods. H. pylori and a human gastric epithelial cell line (AGS) were cocultured. The proliferation of AGS cells was quantitated by an MTT assay, and the expression of HSP70 in AGS cells was detected by Western blotting. HSP70 expression in AGS cells was silenced by small interfering RNA (siRNA) to investigate the role of HSP70. The siRNA-treated AGS cells were cocultured with H. pylori and cell proliferation was measured by an MTT assay. Results. The proliferation of AGS cells was accelerated by coculturing with H. pylori for 4 and 8 h, but was suppressed at 24 and 48 h. HSP70 expression was decreased in AGS cells infected by H. pylori for 48 h. The proliferation in HSP70-silenced AGS cells was inhibited after coculturing with H. pylori for 24 and 48 h compared with the control group. Conclusions. Coculture of H. pylori altered the proliferation of gastric epithelial cells and decreased HSP70 expression. HSP70 knockdown supplemented the inhibitory effect of H. pylori on proliferation of epithelial cells. These results indicate that the effects of H. pylori on the proliferation of gastric epithelial cells at least partially depend on the decreased expression of HSP70 induced by the bacterium. Hindawi Publishing Corporation 2014 2014-08-05 /pmc/articles/PMC4138794/ /pubmed/25161665 http://dx.doi.org/10.1155/2014/794342 Text en Copyright © 2014 Liping Tao et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Article Tao, Liping Zou, Hai Huang, Zhimin Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells |
title | Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells |
title_full | Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells |
title_fullStr | Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells |
title_full_unstemmed | Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells |
title_short | Effects of Helicobacter pylori and Heat Shock Protein 70 on the Proliferation of Human Gastric Epithelial Cells |
title_sort | effects of helicobacter pylori and heat shock protein 70 on the proliferation of human gastric epithelial cells |
topic | Research Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4138794/ https://www.ncbi.nlm.nih.gov/pubmed/25161665 http://dx.doi.org/10.1155/2014/794342 |
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