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The small-molecule formyl peptide receptor biased agonist, compound 17b, is a vasodilator and anti-inflammatory in mouse precision-cut lung slices.

التفاصيل البيبلوغرافية
العنوان: The small-molecule formyl peptide receptor biased agonist, compound 17b, is a vasodilator and anti-inflammatory in mouse precision-cut lung slices.
المؤلفون: Studley WR; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia., Lamanna E; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia., Martin KA; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia., Nold-Petry CA; Department of Paediatrics, Monash University, Clayton, Victoria, Australia.; Ritchie Centre, Hudson Institute of Medical Research, Clayton, Victoria, Australia., Royce SG; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia., Woodman OL; Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia., Ritchie RH; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.; Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia.; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Qin CX; Monash Institute of Pharmaceutical Sciences, Monash University, Parkville, Victoria, Australia.; Baker Heart and Diabetes Institute, Melbourne, Victoria, Australia., Bourke JE; Department of Pharmacology, Biomedicine Discovery Institute, Monash University, Clayton, Victoria, Australia.
المصدر: British journal of pharmacology [Br J Pharmacol] 2024 Jul; Vol. 181 (14), pp. 2287-2301. Date of Electronic Publication: 2023 Sep 26.
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Wiley Country of Publication: England NLM ID: 7502536 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1476-5381 (Electronic) Linking ISSN: 00071188 NLM ISO Abbreviation: Br J Pharmacol Subsets: MEDLINE
أسماء مطبوعة: Publication: London : Wiley
Original Publication: London, Macmillian Journals Ltd.
مواضيع طبية MeSH: Receptors, Formyl Peptide*/agonists , Receptors, Formyl Peptide*/antagonists & inhibitors , Receptors, Formyl Peptide*/metabolism , Mice, Inbred C57BL* , Vasodilator Agents*/pharmacology , Lung*/drug effects , Lung*/metabolism , Anti-Inflammatory Agents*/pharmacology, Animals ; Male ; Mice ; Female ; Dose-Response Relationship, Drug ; Vasodilation/drug effects
مستخلص: Background and Purpose: Pulmonary arterial hypertension (PAH), a rare fatal disorder characterised by inflammation, vascular remodelling and vasoconstriction. Current vasodilator therapies reduce pulmonary arterial pressure but not mortality. The G-protein coupled formyl peptide receptors (FPRs) mediates vasodilatation and resolution of inflammation, actions possibly beneficial in PAH. We investigated dilator and anti-inflammatory effects of the FPR biased agonist compound 17b in pulmonary vasculature using mouse precision-cut lung slices (PCLS).
Experimental Approach: PCLS from 8-week-old male and female C57BL/6 mice, intrapulmonary arteries were pre-contracted with 5-HT for concentration-response curves to compound 17b and 43, and standard-of-care drugs, sildenafil, iloprost and riociguat. Compound 17b-mediated relaxation was assessed with FPR antagonists or inhibitors and in PCLS treated with TNF-α or LPS. Cytokine release from TNF-α- or LPS-treated PCLS ± compound 17b was measured.
Key Results: Compound 17b elicited concentration-dependent vasodilation, with potencies of iloprost > compound 17b = riociguat > compound 43 = sildenafil. Compound 17b was inhibited by the FPR1 antagonist cyclosporin H but not by soluble guanylate cyclase, nitric oxide synthase or cyclooxygenase inhibitors. Under inflammatory conditions, the efficacy and potency of compound 17b were maintained, while iloprost and sildenafil were less effective. Additionally, compound 17b inhibited secretion of PAH-relevant cytokines via FPR2.
Conclusions and Implications: Vasodilation to compound 17b but not standard-of-care vasodilators, is maintained under inflammatory conditions, with additional inhibition of PAH-relevant cytokine release. This provides the first evidence that targeting FPR, with biased agonist, simultaneously targets vascular function and inflammation, supporting the development of FPR-based pharmacotherapy to treat PAH.
Linked Articles: This article is part of a themed issue Therapeutic Targeting of G Protein-Coupled Receptors: hot topics from the Australasian Society of Clinical and Experimental Pharmacologists and Toxicologists 2021 Virtual Annual Scientific Meeting. To view the other articles in this section visit http://onlinelibrary.wiley.com/doi/10.1111/bph.v181.14/issuetoc.
(© 2023 The Authors. British Journal of Pharmacology published by John Wiley & Sons Ltd on behalf of British Pharmacological Society.)
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معلومات مُعتمدة: ID1187989 National Health and Medical Research Council; Victorian Government of Australia's Operational Infrastructure Support Program; National Heart Foundation of Australia Future Leader Fellowship; Australian Government Research Training Program (RTP) Scholarship
فهرسة مساهمة: Keywords: formyl peptide receptor; inflammation; precision‐cut lung slice; pulmonary arterial hypertension; respiratory pharmacology; vasodilation
المشرفين على المادة: 0 (Receptors, Formyl Peptide)
0 (Vasodilator Agents)
0 (Anti-Inflammatory Agents)
تواريخ الأحداث: Date Created: 20230902 Date Completed: 20240619 Latest Revision: 20240625
رمز التحديث: 20240626
DOI: 10.1111/bph.16231
PMID: 37658546
قاعدة البيانات: MEDLINE
الوصف
تدمد:1476-5381
DOI:10.1111/bph.16231