Inhibition of USP14 suppresses the formation of foam cell by promoting CD36 degradation.
Animals
Atherosclerosis
/ pathology
Biological Transport
/ physiology
CD36 Antigens
/ metabolism
Cardiomegaly
/ pathology
Cell Differentiation
/ genetics
Cell Line
Coronary Artery Disease
/ pathology
Foam Cells
/ cytology
Humans
Lipoproteins, LDL
/ metabolism
Macrophages
/ cytology
Mice
Molecular Docking Simulation
RAW 264.7 Cells
RNA Interference
RNA, Small Interfering
/ genetics
Ubiquitin
/ metabolism
Ubiquitin Thiolesterase
/ genetics
Atherosclerosis
CD36
USP14
degradation
foam cell
Journal
Journal of cellular and molecular medicine
ISSN: 1582-4934
Titre abrégé: J Cell Mol Med
Pays: England
ID NLM: 101083777
Informations de publication
Date de publication:
03 2020
03 2020
Historique:
received:
20
08
2019
revised:
19
11
2019
accepted:
29
12
2019
pubmed:
24
1
2020
medline:
10
9
2021
entrez:
24
1
2020
Statut:
ppublish
Résumé
Atherosclerosis is regarded as a chronic progressive inflammatory disease and is a basic pathophysiological process in coronary artery disease which is life threatening in clinic. The formation of foam cell plays a key role in the pathogenesis of atherosclerosis. OxLDL is a significant factor in progression of coronary artery disease. Our studies have demonstrated that USP14 promotes cancer development and mediates progression of cardiac hypertrophy and LPS-induced inflammation. However, the underlying mechanism of USP14 is unknown. In this study, we found that the inhibition of USP14 significantly suppressed the oxLDL uptake, subsequently decreased the foam cell formation. Surprisingly, USP14 has an effect on the expression of CD36 but not SR-A, ABCA1, Lox-1, ABCG1 and SR-Bl. Furthermore, USP14 stabilizes CD36 protein via cleaving the ubiquitin chain on CD36. Blocking CD36 activation using antibody-dependent blocking assay remarkably attenuated the function of USP14 on the formation of foam cell. In summary, our results suggested that the inhibition of USP14 decreases foam cell formation by down-regulating CD36-mediated lipid uptake and provides a potential therapeutic target for atherosclerosis.
Identifiants
pubmed: 31970862
doi: 10.1111/jcmm.15002
pmc: PMC7131911
doi:
Substances chimiques
CD36 Antigens
0
Lipoproteins, LDL
0
RNA, Small Interfering
0
USP14 protein, human
0
Ubiquitin
0
oxidized low density lipoprotein
0
Ubiquitin Thiolesterase
EC 3.4.19.12
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
3292-3302Informations de copyright
© 2020 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.
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