Toll-like receptor 2-deficiency on bone marrow-derived cells augments vascular healing of murine arterial lesions.
Arterial injury
Neointima
Restenosis
Smooth muscle cells
TLR2
Toll-like receptor 2
Journal
Life sciences
ISSN: 1879-0631
Titre abrégé: Life Sci
Pays: Netherlands
ID NLM: 0375521
Informations de publication
Date de publication:
01 Feb 2020
01 Feb 2020
Historique:
received:
12
11
2019
revised:
12
12
2019
accepted:
16
12
2019
pubmed:
1
1
2020
medline:
6
2
2020
entrez:
1
1
2020
Statut:
ppublish
Résumé
Neointimal hyperplasia contributes to arterial restenosis after percutaneous transluminal coronary angioplasty or vascular surgery. Neointimal thickening after arterial injury is determined by inflammatory processes. We investigated the role of the innate immune receptor toll-like receptor 2 (TLR2) in neointima formation after arterial injury in mice. Carotid artery injury was induced by 10% ferric chloride in C57Bl/6J wild type (WT), TLR2 deficient (B6.129-Tlr2 TLR2 TLR2-deficiency on hematopoietic but not vessel wall resident cells augments vascular healing after arterial injury. Pharmacological blockade of TLR2 may thus be a promising therapeutic option to improve vessel patency after iatrogenic arterial injury.
Identifiants
pubmed: 31891724
pii: S0024-3205(19)31117-8
doi: 10.1016/j.lfs.2019.117189
pii:
doi:
Substances chimiques
Tlr2 protein, mouse
0
Toll-Like Receptor 2
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
117189Informations de copyright
Copyright © 2019 Elsevier Inc. All rights reserved.