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Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts
Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechani...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
D.A. Spandidos
2018
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783511/ https://www.ncbi.nlm.nih.gov/pubmed/29257277 http://dx.doi.org/10.3892/mmr.2017.8233 |
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author | Li, Jun Zhang, Yong-Gang Luo, Li-Min Dong, Xiao Ding, Wen-Hui Dang, Shu-Yi |
author_facet | Li, Jun Zhang, Yong-Gang Luo, Li-Min Dong, Xiao Ding, Wen-Hui Dang, Shu-Yi |
author_sort | Li, Jun |
collection | PubMed |
description | Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry. Growth-arrested AFs and tunica adventitia from rat vessels were incubated with UII and inhibitors of various signal transduction pathways. ALD receptor (ALD-R) mRNA expression levels and ALD protein exoression levels were determined by reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. Aldosterone and its receptors were expressed on tunica adventitia. UII promoted ALD protein secretion from cells in a dose- and time-dependent manner. ALD-R mRNA expression in cells was also dysregulated. Furthermore, the effects of UII were substantially inhibited by treatment with the inhibitors PD98059, Y-27632, H-7, CSA and nicardipine. These results were further verified in the tunica adventitia of rat vessels. The present findings indicated that UII stimulated ALD protein secretion and ALD-R mRNA expression in AFs and in the tunica adventitia of rat vessels; moreover, this effect may be mediated by signal transduction pathways involving MAPK, Rho, PKC, calcineurin and Ca(2+). UII may also contribute to vascular remodeling by stimulating the production of ALD and its receptor. |
format | Online Article Text |
id | pubmed-5783511 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2018 |
publisher | D.A. Spandidos |
record_format | MEDLINE/PubMed |
spelling | pubmed-57835112018-02-12 Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts Li, Jun Zhang, Yong-Gang Luo, Li-Min Dong, Xiao Ding, Wen-Hui Dang, Shu-Yi Mol Med Rep Articles Urotensin II (UII) contributes to cardiovascular diseases by activating vasoactive peptides. The present study aimed to determine the effect of UII on aldosterone (ALD) and its receptor in cultured adventitial fibroblasts (AFs) and the tunica adventitia of rat vessels to explore the possible mechanisms underlying vascular remodeling. Expression levels of aldosterone and its receptor on tunica adventitia were determined using immunohistochemistry. Growth-arrested AFs and tunica adventitia from rat vessels were incubated with UII and inhibitors of various signal transduction pathways. ALD receptor (ALD-R) mRNA expression levels and ALD protein exoression levels were determined by reverse transcription-quantitative polymerase chain reaction and ELISA, respectively. Aldosterone and its receptors were expressed on tunica adventitia. UII promoted ALD protein secretion from cells in a dose- and time-dependent manner. ALD-R mRNA expression in cells was also dysregulated. Furthermore, the effects of UII were substantially inhibited by treatment with the inhibitors PD98059, Y-27632, H-7, CSA and nicardipine. These results were further verified in the tunica adventitia of rat vessels. The present findings indicated that UII stimulated ALD protein secretion and ALD-R mRNA expression in AFs and in the tunica adventitia of rat vessels; moreover, this effect may be mediated by signal transduction pathways involving MAPK, Rho, PKC, calcineurin and Ca(2+). UII may also contribute to vascular remodeling by stimulating the production of ALD and its receptor. D.A. Spandidos 2018-02 2017-12-08 /pmc/articles/PMC5783511/ /pubmed/29257277 http://dx.doi.org/10.3892/mmr.2017.8233 Text en Copyright: © Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License (https://creativecommons.org/licenses/by-nc-nd/4.0/) , which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made. |
spellingShingle | Articles Li, Jun Zhang, Yong-Gang Luo, Li-Min Dong, Xiao Ding, Wen-Hui Dang, Shu-Yi Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
title | Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
title_full | Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
title_fullStr | Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
title_full_unstemmed | Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
title_short | Urotensin II promotes aldosterone expression in rat aortic adventitial fibroblasts |
title_sort | urotensin ii promotes aldosterone expression in rat aortic adventitial fibroblasts |
topic | Articles |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5783511/ https://www.ncbi.nlm.nih.gov/pubmed/29257277 http://dx.doi.org/10.3892/mmr.2017.8233 |
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