Cargando…
A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression
BACKGROUND: "Phosphatase and tensin homolog deleted on chromosome 10" (PTEN) is mostly considered to be a cancer-related gene, and has been suggested to be a new pathway of pathogenesis of asthma. The purpose of this study was to investigate the effects of the glucocorticoid, dexamethasone...
Autores principales: | , , , , , , , |
---|---|
Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2011
|
Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096598/ https://www.ncbi.nlm.nih.gov/pubmed/21489309 http://dx.doi.org/10.1186/1465-9921-12-47 |
_version_ | 1782203731970883584 |
---|---|
author | Ni, ZhenHua Tang, JiHong Cai, ZhuYing Yang, Wei Zhang, Lei Chen, Qingge Zhang, Long Wang, XiongBiao |
author_facet | Ni, ZhenHua Tang, JiHong Cai, ZhuYing Yang, Wei Zhang, Lei Chen, Qingge Zhang, Long Wang, XiongBiao |
author_sort | Ni, ZhenHua |
collection | PubMed |
description | BACKGROUND: "Phosphatase and tensin homolog deleted on chromosome 10" (PTEN) is mostly considered to be a cancer-related gene, and has been suggested to be a new pathway of pathogenesis of asthma. The purpose of this study was to investigate the effects of the glucocorticoid, dexamethasone, on PTEN regulation. METHODS: OVA-challenged mice were used as an asthma model to investigate the effect of dexamethasone on PTEN regulation. Immunohistochemistry was used to detect expression levels of PTEN protein in lung tissues. The human A549 cell line was used to explore the possible mechanism of action of dexamethasone on human PTEN regulation in vitro. A luciferase reporter construct under the control of PTEN promoter was used to confirm transcriptional regulation in response to dexamethasone. RESULTS: PTEN protein was found to be expressed at low levels in lung tissues in asthmatic mice; but the expression was restored after treatment with dexamethasone. In A549 cells, human PTEN was up-regulated by dexamethasone treatment. The promoter-reporter construct confirmed that dexamethasone could regulate human PTEN transcription. Treatment with the histone deacetylase inhibitor, TSA, could increase PTEN expression in A549 cells, while inhibition of histone acetylase (HAT) by anacardic acid attenuated dexamethasone-induced PTEN expression. CONCLUSIONS: Based on the data a new mechanism is proposed where glucocorticoids treat asthma partly through up-regulation of PTEN expression. The in vitro studies also suggest that the PTEN pathway may be involved in human asthma. |
format | Text |
id | pubmed-3096598 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-30965982011-05-18 A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression Ni, ZhenHua Tang, JiHong Cai, ZhuYing Yang, Wei Zhang, Lei Chen, Qingge Zhang, Long Wang, XiongBiao Respir Res Research BACKGROUND: "Phosphatase and tensin homolog deleted on chromosome 10" (PTEN) is mostly considered to be a cancer-related gene, and has been suggested to be a new pathway of pathogenesis of asthma. The purpose of this study was to investigate the effects of the glucocorticoid, dexamethasone, on PTEN regulation. METHODS: OVA-challenged mice were used as an asthma model to investigate the effect of dexamethasone on PTEN regulation. Immunohistochemistry was used to detect expression levels of PTEN protein in lung tissues. The human A549 cell line was used to explore the possible mechanism of action of dexamethasone on human PTEN regulation in vitro. A luciferase reporter construct under the control of PTEN promoter was used to confirm transcriptional regulation in response to dexamethasone. RESULTS: PTEN protein was found to be expressed at low levels in lung tissues in asthmatic mice; but the expression was restored after treatment with dexamethasone. In A549 cells, human PTEN was up-regulated by dexamethasone treatment. The promoter-reporter construct confirmed that dexamethasone could regulate human PTEN transcription. Treatment with the histone deacetylase inhibitor, TSA, could increase PTEN expression in A549 cells, while inhibition of histone acetylase (HAT) by anacardic acid attenuated dexamethasone-induced PTEN expression. CONCLUSIONS: Based on the data a new mechanism is proposed where glucocorticoids treat asthma partly through up-regulation of PTEN expression. The in vitro studies also suggest that the PTEN pathway may be involved in human asthma. BioMed Central 2011 2011-04-14 /pmc/articles/PMC3096598/ /pubmed/21489309 http://dx.doi.org/10.1186/1465-9921-12-47 Text en Copyright ©2011 Ni et al; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. |
spellingShingle | Research Ni, ZhenHua Tang, JiHong Cai, ZhuYing Yang, Wei Zhang, Lei Chen, Qingge Zhang, Long Wang, XiongBiao A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression |
title | A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression |
title_full | A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression |
title_fullStr | A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression |
title_full_unstemmed | A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression |
title_short | A new pathway of glucocorticoid action for asthma treatment through the regulation of PTEN expression |
title_sort | new pathway of glucocorticoid action for asthma treatment through the regulation of pten expression |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3096598/ https://www.ncbi.nlm.nih.gov/pubmed/21489309 http://dx.doi.org/10.1186/1465-9921-12-47 |
work_keys_str_mv | AT nizhenhua anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT tangjihong anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT caizhuying anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT yangwei anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT zhanglei anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT chenqingge anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT zhanglong anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT wangxiongbiao anewpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT nizhenhua newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT tangjihong newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT caizhuying newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT yangwei newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT zhanglei newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT chenqingge newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT zhanglong newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression AT wangxiongbiao newpathwayofglucocorticoidactionforasthmatreatmentthroughtheregulationofptenexpression |