Resolvin D1 modulates periodontal ligament fibroblast function.


Journal

Journal of periodontology
ISSN: 1943-3670
Titre abrégé: J Periodontol
Pays: United States
ID NLM: 8000345

Informations de publication

Date de publication:
05 2023
Historique:
revised: 05 11 2022
received: 07 09 2022
accepted: 13 11 2022
pmc-release: 01 05 2024
medline: 24 5 2023
pubmed: 24 11 2022
entrez: 23 11 2022
Statut: ppublish

Résumé

The resolution of inflammation is an active process mediated by specialized lipid mediators called lipoxins and resolvins. Periodontal ligament fibroblasts (PDLFs) play a significant role in periodontal regeneration. The purpose of the current study was to determine the impact of resolvin D1 (RvD1) on human PDLF cell wound healing and proliferation, receptor expression (G-protein-coupled receptor 32 [GPR32] and formyl peptide receptor 2 [ALX/FPR2]), and cytokine expression and release. PDLFs were stimulated with interleukin-1β (IL-1β) (500 pg/ml) with and without RvD1 (100 nM). RvD1 receptor expression was determined by quantitative real-time polymerase chain reaction (qPCR), immunofluorescence microscopy, and fluorescence-activated cell sorting. Wound closure was measured by a scratch assay, and proliferation was determined by bromodeoxyuridine incorporation. Interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemoattractant protein-1, cyclooxygenase-2, matrix metalloproteinases-1, -2, and -3 (MMP-1, -2, and -3), tissue inhibitors of metalloproteinases-1 and -2 (TIMP-1 and -2), prostaglandin E2, and osteoprotegerin (OPG) gene expression and production were measured using qPCR and Western blotting, multiplex immunoassay, and enzyme-linked immunosorbent assay. PDLF expressed GPR32 and ALX/FPR2. RvD1 reversed IL-1β-induced inhibition of wound healing and proliferation of PDLF. IL-1β also induced the production of proinflammatory cytokines and MMPs. This effect was reversed by RvD1. RvD1 reversed IL-1β-induced inhibition of TIMP-1, TIMP-2, and OPG. The data suggested that RvD1 has a pro-wound healing, proliferative, and anti-inflammatory impact on the PDLF that favors periodontal regeneration.

Sections du résumé

BACKGROUND
The resolution of inflammation is an active process mediated by specialized lipid mediators called lipoxins and resolvins. Periodontal ligament fibroblasts (PDLFs) play a significant role in periodontal regeneration. The purpose of the current study was to determine the impact of resolvin D1 (RvD1) on human PDLF cell wound healing and proliferation, receptor expression (G-protein-coupled receptor 32 [GPR32] and formyl peptide receptor 2 [ALX/FPR2]), and cytokine expression and release.
METHODS
PDLFs were stimulated with interleukin-1β (IL-1β) (500 pg/ml) with and without RvD1 (100 nM). RvD1 receptor expression was determined by quantitative real-time polymerase chain reaction (qPCR), immunofluorescence microscopy, and fluorescence-activated cell sorting. Wound closure was measured by a scratch assay, and proliferation was determined by bromodeoxyuridine incorporation. Interleukin-6 (IL-6), interleukin-8 (IL-8), monocyte chemoattractant protein-1, cyclooxygenase-2, matrix metalloproteinases-1, -2, and -3 (MMP-1, -2, and -3), tissue inhibitors of metalloproteinases-1 and -2 (TIMP-1 and -2), prostaglandin E2, and osteoprotegerin (OPG) gene expression and production were measured using qPCR and Western blotting, multiplex immunoassay, and enzyme-linked immunosorbent assay.
RESULTS
PDLF expressed GPR32 and ALX/FPR2. RvD1 reversed IL-1β-induced inhibition of wound healing and proliferation of PDLF. IL-1β also induced the production of proinflammatory cytokines and MMPs. This effect was reversed by RvD1. RvD1 reversed IL-1β-induced inhibition of TIMP-1, TIMP-2, and OPG.
CONCLUSION
The data suggested that RvD1 has a pro-wound healing, proliferative, and anti-inflammatory impact on the PDLF that favors periodontal regeneration.

Identifiants

pubmed: 36416879
doi: 10.1002/JPER.22-0462
pmc: PMC10354588
mid: NIHMS1913748
doi:

Substances chimiques

resolvin D1 0
Tissue Inhibitor of Metalloproteinase-1 0
Docosahexaenoic Acids 25167-62-8
Cytokines 0

Types de publication

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

Langues

eng

Sous-ensembles de citation

IM

Pagination

683-693

Subventions

Organisme : NIDCR NIH HHS
ID : R01 DE025020
Pays : United States

Informations de copyright

© 2022 American Academy of Periodontology.

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Auteurs

Ahmed E Zarrough (AE)

Missouri School of Dentistry & Oral Health, A.T. Still University, St. Louis, Missouri, USA.

Hatice Hasturk (H)

Department of Clinical and Translational Research, Forsyth Institute, Cambridge, Massachusetts, USA.

Danielle N Stephens (DN)

Department of Clinical and Translational Research, Forsyth Institute, Cambridge, Massachusetts, USA.

Thomas E Van Dyke (TE)

Department of Clinical and Translational Research, Forsyth Institute, Cambridge, Massachusetts, USA.

Alpdogan Kantarci (A)

Department of Clinical and Translational Research, Forsyth Institute, Cambridge, Massachusetts, USA.

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Classifications MeSH