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Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model
BACKGROUND: Thiazolidinediones exert anti-inflammatory and anti-oxidative roles and attenuate atherosclerosis by mechanisms partially independent of their metabolizing actions. High doses of angiotensin type 1 receptor (AT(1)R) blocker losartan (LST) seem to promote fat cell formation by preserving...
Autores principales: | , , , , |
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Formato: | Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2008
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266907/ https://www.ncbi.nlm.nih.gov/pubmed/18302760 http://dx.doi.org/10.1186/1475-2840-7-3 |
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author | Hernandez-Trujillo, Y Rodriguez-Esparragon, F Macias-Reyes, A Caballero-Hidalgo, A Rodriguez-Perez, Jose C |
author_facet | Hernandez-Trujillo, Y Rodriguez-Esparragon, F Macias-Reyes, A Caballero-Hidalgo, A Rodriguez-Perez, Jose C |
author_sort | Hernandez-Trujillo, Y |
collection | PubMed |
description | BACKGROUND: Thiazolidinediones exert anti-inflammatory and anti-oxidative roles and attenuate atherosclerosis by mechanisms partially independent of their metabolizing actions. High doses of angiotensin type 1 receptor (AT(1)R) blocker losartan (LST) seem to promote fat cell formation by preserving PPARγ activity. METHODS: C57BL/6J diet-induced atherosclerotic susceptible mice randomly received a normal or a high-fat high-cholesterol (HFHC) diet and were treated with rosiglitazone (RG), LST or a vehicle for 12 weeks. RESULTS: HFHC was associated with increased PPARγ gene expression without an over regulation of PPARγ responsive genes, whereas RG and LST treatments were found to maintain PPARγ activity without resulting in increased PPARγ gene expression. A better anti-inflammatory and antioxidant profile in mice treated with RG regarding LST was observed in spite of a similar PPARγ preserved activity. Chromatin immunoprecipitation (ChIP) assays revealed that animals under HFHC diet treated with RG showed a significant nuclear factor erythroid 2-like 2 (Nrf2)-dependent down-regulation of the expression of the CD36 gene. CONCLUSION: The PPARγ agonist RG exerts antioxidant properties that significantly reduced Nrf-2-dependent CD-36 up-regulation in mice under HFHC diet. Because LST treatment was also associated with a preserved PPARγ activity, our data suggests that these RG antioxidant effects are partially independent of its PPARγ metabolizing properties. |
format | Text |
id | pubmed-2266907 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2008 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-22669072008-03-12 Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model Hernandez-Trujillo, Y Rodriguez-Esparragon, F Macias-Reyes, A Caballero-Hidalgo, A Rodriguez-Perez, Jose C Cardiovasc Diabetol Original Investigation BACKGROUND: Thiazolidinediones exert anti-inflammatory and anti-oxidative roles and attenuate atherosclerosis by mechanisms partially independent of their metabolizing actions. High doses of angiotensin type 1 receptor (AT(1)R) blocker losartan (LST) seem to promote fat cell formation by preserving PPARγ activity. METHODS: C57BL/6J diet-induced atherosclerotic susceptible mice randomly received a normal or a high-fat high-cholesterol (HFHC) diet and were treated with rosiglitazone (RG), LST or a vehicle for 12 weeks. RESULTS: HFHC was associated with increased PPARγ gene expression without an over regulation of PPARγ responsive genes, whereas RG and LST treatments were found to maintain PPARγ activity without resulting in increased PPARγ gene expression. A better anti-inflammatory and antioxidant profile in mice treated with RG regarding LST was observed in spite of a similar PPARγ preserved activity. Chromatin immunoprecipitation (ChIP) assays revealed that animals under HFHC diet treated with RG showed a significant nuclear factor erythroid 2-like 2 (Nrf2)-dependent down-regulation of the expression of the CD36 gene. CONCLUSION: The PPARγ agonist RG exerts antioxidant properties that significantly reduced Nrf-2-dependent CD-36 up-regulation in mice under HFHC diet. Because LST treatment was also associated with a preserved PPARγ activity, our data suggests that these RG antioxidant effects are partially independent of its PPARγ metabolizing properties. BioMed Central 2008-02-26 /pmc/articles/PMC2266907/ /pubmed/18302760 http://dx.doi.org/10.1186/1475-2840-7-3 Text en Copyright © 2008 Hernandez-Trujillo 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 | Original Investigation Hernandez-Trujillo, Y Rodriguez-Esparragon, F Macias-Reyes, A Caballero-Hidalgo, A Rodriguez-Perez, Jose C Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model |
title | Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model |
title_full | Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model |
title_fullStr | Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model |
title_full_unstemmed | Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model |
title_short | Rosiglitazone but not losartan prevents Nrf-2 dependent CD36 gene expression up-regulation in an in vivo atherosclerosis model |
title_sort | rosiglitazone but not losartan prevents nrf-2 dependent cd36 gene expression up-regulation in an in vivo atherosclerosis model |
topic | Original Investigation |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2266907/ https://www.ncbi.nlm.nih.gov/pubmed/18302760 http://dx.doi.org/10.1186/1475-2840-7-3 |
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