FPR2 DNA Aptamers for Targeted Therapy of Wound Repair.
Journal
The Journal of investigative dermatology
ISSN: 1523-1747
Titre abrégé: J Invest Dermatol
Pays: United States
ID NLM: 0426720
Informations de publication
Date de publication:
08 2022
08 2022
Historique:
received:
07
07
2020
revised:
14
10
2021
accepted:
21
10
2021
pubmed:
4
1
2022
medline:
27
7
2022
entrez:
3
1
2022
Statut:
ppublish
Résumé
Chronic wounds represent a major health problem worldwide. Some of the available therapies based on recombinant proteins usually fail owing to the hostile environment found at the wound bed. Aptamers appear as an attractive alternative to recombinant factors owing in part to their stability, sensitivity, specificity, and low-cost production. In this study, the Cell-Systematic Evolution of Ligands by EXponential Enrichment technology was employed to generate aptamers that specifically recognize and modulate the function of the FPR2, a receptor expressed in a variety of cells involved in wound repair. Three aptamers were obtained that specifically bound to FPR2 stable transfectants generated in HaCaT cells. The targeted aptamers were shown to act as FPR2 agonists in different in vitro functional assays, including wound healing assays, and elicited a similar pattern of response to that obtained with other known FPR2 peptide agonists, such as the human LL37 cathelicidin. We have also obtained in vivo evidence for the prohealing activities of one of these FPR2 aptamers in a skin-humanized mouse model developed by us, previously shown to accurately recreate the main phases of physiological human wound repair process. In conclusion, we provide evidence of the potential therapeutic value of FPR2 aptamers for cutaneous repair.
Identifiants
pubmed: 34979109
pii: S0022-202X(21)02688-9
doi: 10.1016/j.jid.2021.12.026
pii:
doi:
Substances chimiques
Aptamers, Nucleotide
0
FPR2 protein, human
0
Ligands
0
Receptors, Formyl Peptide
0
Receptors, Lipoxin
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
2238-2248.e8Informations de copyright
Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.