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Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway
Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. The present study aimed to investigate the roles of the...
Autores principales: | , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Impact Journals LLC
2017
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707082/ https://www.ncbi.nlm.nih.gov/pubmed/29221188 http://dx.doi.org/10.18632/oncotarget.21712 |
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author | Shen, Lili Zhang, Tiancheng Lu, Hongyan |
author_facet | Shen, Lili Zhang, Tiancheng Lu, Hongyan |
author_sort | Shen, Lili |
collection | PubMed |
description | Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. The present study aimed to investigate the roles of the AGT in the progression of broncopulmonary dysplasia in premature newborns. By bioinformatics analysis, AGT was found to be the major node in molecular interaction networks of BPD mouse model. Quantitative PCR and western blot analyses were applied to examine AGT expression in A549 cells which were treated with the hyperoxic condition. The AGT inhibitor Valsartan and the AGT agonist ANGII were employed to investigate the roles of AGT in cell growth and the inflammation. Results show that hyperoxic treatment induced upregulation of AGT expression in A549 cells. Overexpression of AGT resulted in the inflammation via the JAK/STAT signal pathway, ultimately suppressed the proliferation of the A549 cell. In conclusion, increased expression of AGT was demonstrated to be associated with the development and progression of BPD, and may be regarded as a promising therapeutic target for BPD. |
format | Online Article Text |
id | pubmed-5707082 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2017 |
publisher | Impact Journals LLC |
record_format | MEDLINE/PubMed |
spelling | pubmed-57070822017-12-07 Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway Shen, Lili Zhang, Tiancheng Lu, Hongyan Oncotarget Research Paper Angiotensinogen (AGT) is involved in the production of angiotensin II which is the main mediator of action of the rennin-angiotensin system (RAS), whereas the RAS mediates the regulation of sodium homeostasis, blood pressure, and inflammation. The present study aimed to investigate the roles of the AGT in the progression of broncopulmonary dysplasia in premature newborns. By bioinformatics analysis, AGT was found to be the major node in molecular interaction networks of BPD mouse model. Quantitative PCR and western blot analyses were applied to examine AGT expression in A549 cells which were treated with the hyperoxic condition. The AGT inhibitor Valsartan and the AGT agonist ANGII were employed to investigate the roles of AGT in cell growth and the inflammation. Results show that hyperoxic treatment induced upregulation of AGT expression in A549 cells. Overexpression of AGT resulted in the inflammation via the JAK/STAT signal pathway, ultimately suppressed the proliferation of the A549 cell. In conclusion, increased expression of AGT was demonstrated to be associated with the development and progression of BPD, and may be regarded as a promising therapeutic target for BPD. Impact Journals LLC 2017-10-10 /pmc/articles/PMC5707082/ /pubmed/29221188 http://dx.doi.org/10.18632/oncotarget.21712 Text en Copyright: © 2017 Shen et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License 3.0 (http://creativecommons.org/licenses/by/3.0/) (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. |
spellingShingle | Research Paper Shen, Lili Zhang, Tiancheng Lu, Hongyan Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway |
title | Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway |
title_full | Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway |
title_fullStr | Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway |
title_full_unstemmed | Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway |
title_short | Overexpression of AGT promotes bronchopulmonary dysplasis via the JAK/STAT signal pathway |
title_sort | overexpression of agt promotes bronchopulmonary dysplasis via the jak/stat signal pathway |
topic | Research Paper |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5707082/ https://www.ncbi.nlm.nih.gov/pubmed/29221188 http://dx.doi.org/10.18632/oncotarget.21712 |
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