Specialized Pro-resolving Mediator Improves Vascular Relaxation via Formyl Peptide Receptor-2.

Animals Mice Rats Acetylcholine Docosahexaenoic Acids / pharmacology Endothelial Cells Inflammation Inflammation Mediators Receptors, Formyl Peptide
blood pressure endothelial dysfunction hypertension resolution of inflammation

Journal

American journal of hypertension
ISSN: 1941-7225
Titre abrégé: Am J Hypertens
Pays: United States
ID NLM: 8803676

Informations de publication

Date de publication:
15 09 2023
Historique:
received: 17 02 2023
revised: 29 06 2023
accepted: 11 07 2023
pmc-release: 13 07 2024
medline: 18 9 2023
pubmed: 13 7 2023
entrez: 13 7 2023
Statut: ppublish

Résumé

The resolution of inflammation is an active phenomenon important for switching off inflammatory processes once the harmful stimuli are removed and facilitate the return to homeostasis. Specialized pro-resolving mediators (SPMs), such as lipoxin A4, resolvin D1, and resolvin E1, derived from ω-3 or ω-6 polyunsaturated fatty acids, are crucial for the resolution of inflammation. We hypothesized that SPMs are decreased in hypertension which contributes to the acetylcholine-induced contraction in resistance arteries, which are well known to be mediated by leukotrienes and prostaglandins. Moreover, treatment with SPMs will decrease this contraction via formyl peptide receptor-2 (FPR-2) in resistance arteries from spontaneously hypertensive rats (SHR). We performed a comprehensive eicosanoid lipid panel analysis, and our data showed for the first time that precursors of SPMs are decreased in SHR, limiting the production of SPMs and resolution of inflammation in vivo. This phenomenon was associated with an increase in lipid peroxidation in resistance arteries. Although SPMs did not abolish acetylcholine-induced contraction, these lipid mediators improved endothelial function in arteries from SHR via FPR-2 activation at nanomolar concentrations. SPMs also buffered TNF-α-induced reactive oxygen species generation in endothelial cells from C57Bl/6 mice. We suggest that FPR-2 and SPMs could be revealed as a new target or therapeutic agent to improve vascular function in arteries from hypertensive rats.

Sections du résumé

BACKGROUND
The resolution of inflammation is an active phenomenon important for switching off inflammatory processes once the harmful stimuli are removed and facilitate the return to homeostasis. Specialized pro-resolving mediators (SPMs), such as lipoxin A4, resolvin D1, and resolvin E1, derived from ω-3 or ω-6 polyunsaturated fatty acids, are crucial for the resolution of inflammation. We hypothesized that SPMs are decreased in hypertension which contributes to the acetylcholine-induced contraction in resistance arteries, which are well known to be mediated by leukotrienes and prostaglandins. Moreover, treatment with SPMs will decrease this contraction via formyl peptide receptor-2 (FPR-2) in resistance arteries from spontaneously hypertensive rats (SHR).
METHODS AND RESULTS
We performed a comprehensive eicosanoid lipid panel analysis, and our data showed for the first time that precursors of SPMs are decreased in SHR, limiting the production of SPMs and resolution of inflammation in vivo. This phenomenon was associated with an increase in lipid peroxidation in resistance arteries. Although SPMs did not abolish acetylcholine-induced contraction, these lipid mediators improved endothelial function in arteries from SHR via FPR-2 activation at nanomolar concentrations. SPMs also buffered TNF-α-induced reactive oxygen species generation in endothelial cells from C57Bl/6 mice.
CONCLUSIONS
We suggest that FPR-2 and SPMs could be revealed as a new target or therapeutic agent to improve vascular function in arteries from hypertensive rats.

Identifiants

DOI: 10.1093/ajh/hpad062 PMID: 37439351 PMC: PMC10502783
pubmed: 37439351
pii: 7223631
doi: 10.1093/ajh/hpad062
pmc: PMC10502783
doi:

Substances chimiques

Acetylcholine N9YNS0M02X
Docosahexaenoic Acids 25167-62-8
Inflammation Mediators 0
Receptors, Formyl Peptide 0
formyl peptide receptor 2, mouse 0

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

542-550

Subventions

Organisme : NIGMS NIH HHS
ID : P20 GM103641
Pays : United States
Organisme : NHLBI NIH HHS
ID : P01 HL134604
Pays : United States
Organisme : NHLBI NIH HHS
ID : R00 HL151889
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL149762
Pays : United States
Organisme : NIGMS NIH HHS
ID : R00 GM118885
Pays : United States

Informations de copyright

© The Author(s) 2023. Published by Oxford University Press on behalf of American Journal of Hypertension, Ltd. All rights reserved. For permissions, please e-mail: journals.permissions@oup.com.

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Auteurs

Jonnelle M Edwards-Glenn (JM)

Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.

Milene T Fontes (MT)

Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.

Emily W Waigi (EW)

Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.

Tiago J Costa (TJ)

Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.

Andrei Maiseyeu (A)

Cardiovascular Research Institute, Case Western Reserve University School of Medicine, Cleveland, Ohio, USA.

R Clinton Webb (RC)

Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Biomedical Engineering Program, College of Engineering and Computing, University of South Carolina, Columbia, South Carolina, USA.

Cameron G McCarthy (CG)

Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Biomedical Engineering Program, College of Engineering and Computing, University of South Carolina, Columbia, South Carolina, USA.

Camilla F Wenceslau (CF)

Cardiovascular Translational Research Center, Department of Cell Biology and Anatomy, University of South Carolina School of Medicine, Columbia, South Carolina, USA.
Biomedical Engineering Program, College of Engineering and Computing, University of South Carolina, Columbia, South Carolina, USA.
ORCID: 0000-0002-0815-3568

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Classifications MeSH

Recherchemedicale.com › Eucaryotes › Animaux › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Souris › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Eucaryotes › Animaux › Chordés › Vertébrés › Mammifères › Eutheria › Rodentia › Muridae › Murinae › Rats › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Composés chimiques organiques › Amines › Amines biogènes › Acétylcholine › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Lipides › Huiles › Huiles de poisson › Acides gras omega-3 › Acide docosahexaénoïque › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Cellules › Cellules épithéliales › Cellules endothéliales › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › États, signes et symptômes pathologiques › Processus pathologiques › Inflammation › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Facteurs biologiques › Médiateurs de l'inflammation › Specialized Pro-resolving Mediator Improves...
Recherchemedicale.com › Acides aminés, peptides et protéines › Protéines › Protéines membranaires › Récepteurs de surface cellulaire › Récepteurs peptidiques › Récepteurs aux peptides formylés › Specialized Pro-resolving Mediator Improves...