Evidence for the involvement of TRPV2 channels in the modulation of vascular tone in the mouse aorta
Peralvarez-Marin, Alex (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Solé Piñol, Montserrat (Universitat Autònoma de Barcelona. Departament de Bioquímica i de Biologia Molecular)
Serrano, Judith (Universitat Autònoma de Barcelona. Institut de Neurociències)
Taddeucci, Alice (Universitat Autònoma de Barcelona. Institut de Neurociències)
Perez, Belen (Universitat Autònoma de Barcelona. Departament de Farmacologia, de Terapèutica i de Toxicologia)
Penas Pérez, Clara (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia)
Manich, Gemma (Universitat Autònoma de Barcelona. Departament de Ciències Morfològiques)
Jimenez, Marcel (Universitat Autònoma de Barcelona. Departament de Biologia Cel·lular, de Fisiologia i d'Immunologia)
D'Ocon, Pilar (Universitat de València)
Jiménez Altayó, Francesc (Universitat Autònoma de Barcelona. Departament de Farmacologia, de Terapèutica i de Toxicologia)

Date:	2024
Description:	13 pàg.
Abstract:	Aims: Transient receptor potential vanilloid 2 (TRPV2) channels are expressed in both smooth muscle and endothelial cells and participate in vascular mechanotransduction and sensing of high temperatures and lipids. Nevertheless, the impact of TRPV2 channel activation by agonists on the coordinated and cell-type specific modulation of vasoreactivity is unknown. Main methods: Aorta from 2-to 4-months-old male Oncins France 1 mice was dissected and mounted in tissue baths for isometric tension measurements. TRPV2 channel expression was assessed by immunofluorescence and western blot in mice aortas and in cultured A7r5 rat aortic smooth muscle cells. Key findings: TRPV2 channels were expressed in all three mouse aorta layers. Activation of TRPV2 channels with probenecid evoked endothelium-dependent relaxations through a mechanism that involved activation of smooth muscle Kir and Kv channels. In addition, TRPV2 channel inhibition with tranilast increased endothelium-independent relaxations to probenecid and this effect was abrogated by the KATP channel blocker glibenclamide, revealing that smooth muscle TRPV2 channels induce negative feedback on probenecid relaxations mediated via KATP channel inhibition. Exposure to the NO donor sodium nitroprusside increased TRPV2 channel translocation to the plasma membrane in cultured smooth muscle cells and enhanced negative feedback on probenecid relaxations. Significance: In conclusion, we present the first evidence that TRPV2 channels may modulate vascular tone through a balance of opposed inputs from the endothelium and the smooth muscle leading to net vasodilation. The fact that TRPV2 channel-induced activity can be amplified by NO emphasizes the pathophysiological relevance of these findings.
Grants:	Agencia Estatal de Investigación PID2020-113634RB-C22 Agencia Estatal de Investigación PID2020-120222GB-I00
Note:	Altres ajuts: acords transformatius de la UAB
Rights:	Aquest document està subjecte a una llicència d'ús Creative Commons. Es permet la reproducció total o parcial, la distribució, la comunicació pública de l'obra i la creació d'obres derivades, fins i tot amb finalitats comercials, sempre i quan es reconegui l'autoria de l'obra original.
Language:	Anglès
Document:	Article ; recerca ; Versió publicada
Subject:	TRPV2 channels ; Mouse aorta ; Endothelium-dependent and independent ; Vasodilatation ; Potassium ion channels ; Nitric oxide ; KATP channels
Published in:	Life Sciences, Vol. 336 (2024) , ISSN 1879-0631

DOI: 10.1016/j.lfs.2023.122286
PMID: 38007144

13 p, 6.3 MB

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