PR1P, a VEGF-stabilizing peptide, reduces injury and inflammation in acute lung injury and ulcerative colitis animal models.
Animals
Mice
Rats
Acute Lung Injury
/ metabolism
Colitis, Ulcerative
/ drug therapy
Cytokines
/ metabolism
Disease Models, Animal
Inflammation
/ chemically induced
Interleukin-6
Peptide Hydrolases
Peptides
/ adverse effects
Respiratory Distress Syndrome
/ metabolism
Vascular Endothelial Growth Factor A
/ metabolism
ARDS
Acute Lung Injury, (ALI)
PR1P
VEGF
inflammation
ulcerative colitis
Journal
Frontiers in immunology
ISSN: 1664-3224
Titre abrégé: Front Immunol
Pays: Switzerland
ID NLM: 101560960
Informations de publication
Date de publication:
2023
2023
Historique:
received:
17
02
2023
accepted:
12
04
2023
medline:
17
5
2023
pubmed:
16
5
2023
entrez:
15
5
2023
Statut:
epublish
Résumé
Acute Respiratory Distress Syndrome (ARDS) and Ulcerative Colitis (UC) are each characterized by tissue damage and uncontrolled inflammation. Neutrophils and other inflammatory cells play a primary role in disease progression by acutely responding to direct and indirect insults to tissue injury and by promoting inflammation through secretion of inflammatory cytokines and proteases. Vascular Endothelial Growth Factor (VEGF) is a ubiquitous signaling molecule that plays a key role in maintaining and promoting cell and tissue health, and is dysregulated in both ARDS and UC. Recent evidence suggests a role for VEGF in mediating inflammation, however, the molecular mechanism by which this occurs is not well understood. We recently showed that PR1P, a 12-amino acid peptide that binds to and upregulates VEGF, stabilizes VEGF from degradation by inflammatory proteases such as elastase and plasmin thereby limiting the production of VEGF degradation products (fragmented VEGF (fVEGF)). Here we show that fVEGF is a neutrophil chemoattractant
Identifiants
pubmed: 37187742
doi: 10.3389/fimmu.2023.1168676
pmc: PMC10175756
doi:
Substances chimiques
Cytokines
0
Interleukin-6
0
Peptide Hydrolases
EC 3.4.-
Peptides
0
Vascular Endothelial Growth Factor A
0
PR1P peptide
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
1168676Informations de copyright
Copyright © 2023 Adini, Ko, Puder, Louie, Kim, Baron and Matthews.
Déclaration de conflit d'intérêts
JB was employed by Janus Biotherapeutics, Inc. BM declares that he is currently a medical consultant to Orpheus Inc. which now owns the IP to PR1P. The remaining authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
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