Pioglitazone reduces angiotensin II-induced COX-2 expression through inhibition of ROS production and ET-1 transcription in vascular cells from spontaneously hypertensive rats
dc.contributor.author | Pérez-Girón, José V | |
dc.contributor.author | Palacios-Ramírez, R | |
dc.contributor.author | Martín, Ángela | |
dc.contributor.author | Hernanz, Raquel | |
dc.contributor.author | Aguado, Andrea | |
dc.contributor.author | Martínez-Revelles, Sonia | |
dc.contributor.author | Barrús, María T | |
dc.contributor.author | Salaices, Mercedes | |
dc.contributor.author | Alonso, María J | |
dc.date.accessioned | 2024-06-04T07:27:15Z | |
dc.date.available | 2024-06-04T07:27:15Z | |
dc.date.issued | 2014-01-01 | |
dc.description.abstract | Glitazones have anti-inflamma-tory properties by interfering with the transcription of proinflamma-tory genes, such as cyclooxygenase (COX)-2, and with ROS produc-tion, which are increased in hypertension. This study analyzedwhether pioglitazone modulates COX-2 expression in hypertension byinterfering with ROS and endothelin (ET)-1. In vivo, pioglitazone (2.5mg·kg 1 ·day 1 , 28 days) reduced the greater levels of COX-2,pre-pro-ET-1, and NADPH oxidase (NOX) expression and activity aswell as O2· production found in aortas from spontaneously hyper-tensive rats (SHRs). ANG II increased COX-2 and pre-pro-ET-1levels more in cultured vascular smooth muscle cells from hyperten-sive rats compared with normotensive rats. The ETA receptor antag-onist BQ-123 reduced ANG II-induced COX-2 expression in SHRcells. ANG II also increased NOX-1 expression, NOX activity, andsuperoxide production in SHR cells; the selective NOX-1 inhibitorML-171 and catalase reduced ANG II-induced COX-2 and ET-1transcription. ANG II also increased c-Jun transcription and phospho-JNK1/2, phospho-c-Jun, and p65 NF- B subunit nuclear proteinexpression. SP-600125 and lactacystin, JNK and NF- B inhibitors,respectively, reduced ANG II-induced ET-1, COX-2, and NOX-1levels and NOX activity. Pioglitazone reduced the effects of ANG IIon NOX activity, NOX-1, pre-pro-ET-1, COX-2, and c-Jun mRNAlevels, JNK activation, and nuclear phospho-c-Jun and p65 expres-sion. In conclusion, ROS production and ET-1 are involved in ANGII-induced COX-2 expression in SHRs, explaining the greater COX-2expression observed in this strain. Furthermore, pioglitazone inhibitsANG II-induced COX-2 expression likely by interfering with NF- Band activator protein-1 proinflammatory pathways and downregulat-ing ROS production and ET-1 transcription, thus contributing to theanti-inflammatory properties of glitazones. | es |
dc.identifier.citation | Pioglitazone reduces angiotensin II-induced COX-2 expression through inhibition of ROS production and ET-1 transcription in vascular cells from spontaneously hypertensive rats Jose V. Pérez-Girón, Roberto Palacios, Angela Martín, Raquel Hernanz, Andrea Aguado, Sonia Martínez-Revelles, María T. Barrús, Mercedes Salaices, and María J. Alonso American Journal of Physiology-Heart and Circulatory Physiology 2014 306:11, H1582-H1593 | es |
dc.identifier.doi | 10.1152/ajpheart.00924.2013 | es |
dc.identifier.issn | 1522-1539 (online) | |
dc.identifier.issn | 0363-6135 (print) | |
dc.identifier.uri | https://hdl.handle.net/10115/33336 | |
dc.language.iso | eng | es |
dc.publisher | American Physiological Society | es |
dc.rights.accessRights | info:eu-repo/semantics/closedAccess | es |
dc.subject | angiotensin II; endothelin-1; reactive oxygen species; cyclooxygenase-2; hypertension; peroxisome proliferator-activated receptor-gamma | es |
dc.title | Pioglitazone reduces angiotensin II-induced COX-2 expression through inhibition of ROS production and ET-1 transcription in vascular cells from spontaneously hypertensive rats | es |
dc.type | info:eu-repo/semantics/article | es |
Archivos
Bloque original
1 - 1 de 1
No hay miniatura disponible
- Nombre:
- 2014 AmJPhysiol-HeartCirc 306 H1582–H1593.pdf
- Tamaño:
- 2.63 MB
- Formato:
- Adobe Portable Document Format
- Descripción:
Bloque de licencias
1 - 1 de 1
No hay miniatura disponible
- Nombre:
- license.txt
- Tamaño:
- 2.67 KB
- Formato:
- Item-specific license agreed upon to submission
- Descripción: