PCTR1 Enhances Repair and Bacterial Clearance in Skin Wounds.
Journal
The American journal of pathology
ISSN: 1525-2191
Titre abrégé: Am J Pathol
Pays: United States
ID NLM: 0370502
Informations de publication
Date de publication:
06 2021
06 2021
Historique:
received:
16
09
2020
revised:
04
02
2021
accepted:
12
02
2021
pubmed:
11
3
2021
medline:
24
7
2021
entrez:
10
3
2021
Statut:
ppublish
Résumé
Tissue injury elicits an inflammatory response that facilitates host defense. Resolution of inflammation promotes the transition to tissue repair and is governed, in part, by specialized pro-resolving mediators (SPM). The complete structures of a novel series of cysteinyl-SPM (cys-SPM) were recently elucidated, and proved to stimulate tissue regeneration in planaria and resolve acute inflammation in mice. Their functions in mammalian tissue repair are of interest. Here, nine structurally distinct cys-SPM were screened and PCTR1 uniquely enhanced human keratinocyte migration with efficacy similar to epidermal growth factor. In skin wounds of mice, PCTR1 accelerated closure. Wound infection increased PCTR1 that coincided with decreased bacterial burden. Addition of PCTR1 reduced wound bacteria levels and decreased inflammatory monocytes/macrophages, which was coupled with increased expression of genes involved in host defense and tissue repair. These results suggest that PCTR1 is a novel regulator of host defense and tissue repair, which could inform new approaches for therapeutic management of delayed tissue repair and infection.
Identifiants
pubmed: 33689792
pii: S0002-9440(21)00082-1
doi: 10.1016/j.ajpath.2021.02.015
pmc: PMC8176141
pii:
doi:
Substances chimiques
Inflammation Mediators
0
Docosahexaenoic Acids
25167-62-8
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
1049-1063Subventions
Organisme : NIGMS NIH HHS
ID : P01 GM095467
Pays : United States
Informations de copyright
Copyright © 2021 American Society for Investigative Pathology. Published by Elsevier Inc. All rights reserved.
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