ArticleThe Journal of biological chemistry2015
Inhibition of Glutathione Production Induces Macrophage CD36 Expression and Enhances Cellular-oxidized Low Density Lipoprotein (oxLDL) Uptake.
Article in The Journal of biological chemistry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 54 citations in OpenAlex.
- CXCL16-dependent scavenging of oxidized lipids by islet macrophages promotes differentiation of pathogenic CD8Immunity · 2024Article
- Sonodynamic therapy for the treatment of atherosclerosis.Journal of pharmaceutical analysis · 2024Review
- CD36 inhibition reduces non-small-cell lung cancer development through AKT-mTOR pathway.Cell biology and toxicology · 2024Article
- The function of CD36 inFrontiers in immunology · 2024Review
- Fisetin treatment alleviates kidney injury in mice with diabetes-exacerbated atherosclerosis through inhibiting CD36/fibrosis pathway.Acta pharmacologica Sinica · 2023Article
- Transaldolase inhibits CD36 expression by modulating glutathione-p38 signaling, exerting protective effects against macrophage foam cell formation.Acta biochimica et biophysica Sinica · 2023Article
- Plasma levels of CD36 and glutathione as biomarkers for ruptured intracranial aneurysm.Open life sciences · 2023Article
- Induction of glutathione biosynthesis by glycine-based treatment mitigates atherosclerosis.Redox biology · 2022Article
- Combination of Colchicine and Ticagrelor Inhibits Carrageenan-Induced Thrombi in Mice.Oxidative medicine and cellular longevity · 2022Article
- The Role of Peroxisome Proliferator-Activated Receptor Gamma and Atherosclerosis: Post-translational Modification and Selective Modulators.Frontiers in physiology · 2022Review
- Redox regulation of hemodynamics response to diadenosine tetraphosphate an agonist of P2 receptors and renal function in diet-induced hypercholesterolemic rats.Physiological reports · 2021Article
- Peroxisome Proliferator-Activated Receptor-Gamma Reduces ER Stress and Inflammation via Targeting NGBR Expression.Frontiers in pharmacology · 2021Article
- S-glutathionylation, friend or foe in cardiovascular health and disease.Redox biology · 2020Review
- Inhibition of USP14 suppresses the formation of foam cell by promoting CD36 degradation.Journal of cellular and molecular medicine · 2020Article
- Glutathione Synthesis Contributes to Virulence ofJournal of bacteriology · 2019Article
- Macrophage fatty acid oxidation inhibits atherosclerosis progression.Journal of molecular and cellular cardiology · 2019Article
- Dehydrocostus lactone suppresses ox-LDL-induced attachment of monocytes to endothelial cells.American journal of translational research · 2019Article
- Metabolic Dysfunction and Peroxisome Proliferator-Activated Receptors (PPAR) in Multiple Sclerosis.International journal of molecular sciences · 2018Review
- Stability Profiles and Therapeutic Effect of Cu/Zn Superoxide Dismutase Chemically Coupled to O-Quaternary Chitosan Derivatives against Dextran Sodium Sulfate-Induced Colitis.International journal of molecular sciences · 2017Article
- Berberine-sonodynamic therapy induces autophagy and lipid unloading in macrophage.Cell death & disease · 2017Article
Corrections and comments
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Authors and funding
11 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The glutathione (GSH)-dependent antioxidant system has been demonstrated to inhibit atherosclerosis. Macrophage CD36 uptakes oxidized low density lipoprotein (oxLDL) thereby facilitating foam cell formation and development of atherosclerosis. It remains unknown if GSH can influence macrophage CD36 expression and cellular oxLDL uptake directly. Herein we report that treatment of macrophages with l-buthionine-S,R-sulfoximine (BSO) decreased cellular GSH production and ratios of GSH to glutathione disulfide (GSH/GSSG) while increasing production of reactive oxygen species. Associated with decreased GSH levels, macrophage CD36 expression was increased, which resulted in enhanced cellular oxLDL uptake. In contrast, N-acetyl cysteine and antioxidant enzyme (catalase or superoxide dismutase) blocked BSO-induced CD36 expression as well as oxLDL uptake. In vivo, administration of mice with BSO increased CD36 expression in peritoneal macrophages and kidneys. BSO had no effect on CD36 mRNA expression and promoter activity but still induced CD36 protein expression in macrophages lacking peroxisome proliferator-activated receptor γ expression, suggesting it induced CD36 expression at the translational level. Indeed, we determined that BSO enhanced CD36 translational efficiency. Taken together, our study demonstrates that cellular GSH levels and GSH/GSSG status can regulate macrophage CD36 expression and cellular oxLDL uptake and demonstrate an important anti-atherogenic function of the GSH-dependent antioxidant system by providing a novel molecular mechanism.
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