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Toll-like receptor 4 contributes to vascular remodelling and endothelial dysfunction in angiotensin II-induced hypertension

Author
Hernanz, R.; Martínez-Revelles, Sonia; Palacios, R.; Martín, A.; Cachofeiro, V.; Aguado Gómez, Alfredountranslated; García-Redondo, L.; Barrús, M. T.; De Batista, P. R.; Briones Alonso, Ana Maríauntranslated; Salaices Sánchez, Mercedesuntranslated; Alonso, M. J.
Entity
UAM. Departamento de Farmacología; Instituto de Investigación Sanitaria Hospital Universitario de La Paz (IdiPAZ)
Publisher
The British Pharmacological Society
Date
2015-06-01
Citation
10.1111/bph.13117
British Journal of Pharmacology 172.12 (2015): 3159–3176
 
 
 
ISSN
0007-1188 (print); 1476-5381 (on line)
DOI
10.1111/bph.13117
Funded by
This work was supported by Ministerio de Economía y Competitividad (SAF2012-36400), Instituto de Salud Carlos III (Red de Investigación Cardiovascular RD12/0042/0024 and RD12/0042/0033) and URJC (PRIN13_CS12). AMB was supported by the Ramón y Cajal Program (RYC-2010-06473).
Project
Gobierno de España. SAF2012-36400; Gobierno de España. RYC-2010-06473
Editor's Version
http://dx.doi.org/10.1111/bph.13117
Subjects
TLR4; Hypertension; Oxidative stress; Vascular remodeling; Endothelial dysfunction; Farmacia
URI
http://hdl.handle.net/10486/671180
Note
This is the peer-reviewed version of the following article: "Toll-like receptor 4 contributes to vascular remodelling and endothelial dysfunction in angiotensin II-induced hypertension", British Journal of Pharmacology 172.12 (2015): 3159-76 which has been published in final form at http://dx.doi.org/10.1111/bph.13117 This article may be used for non-commercial purposes in accordance with Wiley-VCH Terms and Conditions for Self-Archiving
Rights
© 2015 The British Pharmacological Society.

Abstract

Background and Purpose Toll-like receptor 4 (TLR4) signalling contributes to inflammatory cardiovascular diseases, but its role in hypertension and the associated vascular damage is not known. We investigated whether TLR4 activation contributed to angiotensin II (AngII)-induced hypertension and the associated vascular structural, mechanical and functional alterations. Experimental Approach AngII was infused (1.44 mg·kg−1·day−1, s.c.) for 2 weeks in C57BL6 mice, treated with a neutralizing anti-TLR4 antibody or IgG (1 μg·day−1); systolic BP (SBP) and aortic cytokine levels were measured. Structural, mechanical and contractile properties of aortic and mesenteric arterial segments were measured with myography and histology. RT-PCR and Western blotting were used to analyse these tissues and cultured vascular smooth muscle cells (VSMC) from hypertensive rats (SHR). Key Results Aortic TLR4 mRNA levels were raised by AngII infusion. Anti-TLR4 antibody treatment of AngII-treated mice normalised: (i) increased SBP and TNF-α, IL-6 and CCL2 levels; (ii) vascular structural and mechanical changes; (iii) altered aortic phenylephrine- and ACh-induced responses; (iv) increased NOX-1 mRNA levels, superoxide anion production and NAD(P)H oxidase activity and effects of catalase, apocynin, ML-171 and Mito-TEMPO on vascular responses; and (v) reduced NO release and effects of L-NAME on phenylephrine-induced contraction. In VSMC, the MyD88 inhibitor ST-2825 reduced AngII-induced NAD(P)H oxidase activity. The TLR4 inhibitor CLI-095 reduced AngII-induced increased phospho-JNK1/2 and p65 NF-κB subunit nuclear protein expression. Conclusions and Implications TLR4 up-regulation by AngII contributed to the inflammation, endothelial dysfunction, vascular remodelling and stiffness associated with hypertension by mechanisms involving oxidative stress. MyD88-dependent activation and JNK/NF-κB signalling pathways participated in these alterations
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Google™ Scholar:Hernanz, R. - Martínez-Revelles, Sonia - Palacios, R. - Martín, A. - Cachofeiro, V. - Aguado Gómez, Alfredo - García-Redondo, L. - Barrús, M. T. - De Batista, P. R. - Briones Alonso, Ana María - Salaices Sánchez, Mercedes - Alonso, M. J.

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