NOXA1-dependent NADPH oxidase regulates redox signaling and phenotype of vascular smooth muscle cell during atherogenesis.
Adaptor Proteins, Signal Transducing
Animals
Apolipoproteins E
/ deficiency
Atherosclerosis
/ genetics
Biomarkers
Enzyme Activation
Gene Deletion
Genetic Loci
Kruppel-Like Factor 4
Mice
Mice, Knockout
Mice, Transgenic
Muscle, Smooth, Vascular
/ cytology
Myocytes, Smooth Muscle
/ cytology
NADPH Oxidases
/ metabolism
Organ Specificity
/ genetics
Oxidation-Reduction
Phenotype
Proteins
/ genetics
Reactive Oxygen Species
/ metabolism
Receptors, LDL
/ deficiency
Signal Transduction
Tumor Necrosis Factor-alpha
/ metabolism
Atherosclerosis
KLF4
Macrophage-like cells
NOXA1
Oxidative stress
Smooth muscle cells
Journal
Redox biology
ISSN: 2213-2317
Titre abrégé: Redox Biol
Pays: Netherlands
ID NLM: 101605639
Informations de publication
Date de publication:
02 2019
02 2019
Historique:
received:
19
10
2018
revised:
16
11
2018
accepted:
29
11
2018
pubmed:
24
12
2018
medline:
4
4
2019
entrez:
22
12
2018
Statut:
ppublish
Résumé
Increased reactive oxygen species (ROS) production and inflammation are key factors in the pathogenesis of atherosclerosis. We previously reported that NOX activator 1 (NOXA1) is the critical functional homolog of p67phox for NADPH oxidase activation in mouse vascular smooth muscle cells (VSMC). Here we investigated the effects of systemic and SMC-specific deletion of Noxa1 on VSMC phenotype during atherogenesis in mice. Neointimal hyperplasia following endovascular injury was lower in Noxa1-deficient mice versus the wild-type following endovascular injury. Noxa1 deletion in Apoe
Identifiants
pubmed: 30576919
pii: S2213-2317(18)30976-5
doi: 10.1016/j.redox.2018.11.021
pmc: PMC6302039
pii:
doi:
Substances chimiques
Adaptor Proteins, Signal Transducing
0
Apolipoproteins E
0
Biomarkers
0
Klf4 protein, mouse
0
Kruppel-Like Factor 4
0
Noxa1 protein, mouse
0
Proteins
0
Reactive Oxygen Species
0
Receptors, LDL
0
Tumor Necrosis Factor-alpha
0
NADPH Oxidases
EC 1.6.3.-
Types de publication
Journal Article
Research Support, N.I.H., Extramural
Langues
eng
Sous-ensembles de citation
IM
Pagination
101063Subventions
Organisme : NHLBI NIH HHS
ID : R01 HL111664
Pays : United States
Organisme : NHLBI NIH HHS
ID : R01 HL139842
Pays : United States
Organisme : NIDDK NIH HHS
ID : U2C DK110768
Pays : United States
Informations de copyright
Copyright © 2018. Published by Elsevier B.V.
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