ArticleThe Journal of biological chemistry2011
Vav protein guanine nucleotide exchange factor regulates CD36 protein-mediated macrophage foam cell formation via calcium and dynamin-dependent processes.
Article in The Journal of biological chemistry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 50 citations in OpenAlex.
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.Arteriosclerosis, thrombosis, and vascular biology · 2026Article
- Macrophage PIM1 Drives Atherosclerosis by Enhancing Foam Cell Formation Via CD36.bioRxiv : the preprint server for biology · 2025Article
- Transcriptome Analysis of Potential Genes Involved in Innate Immunity in Mudflat Crab (Animals : an open access journal from MDPI · 2025Article
- Kaempferol regulating macrophage foaming and atherosclerosis through Piezo1-mediated MAPK/NF-κB and Nrf2/HO-1 signaling pathway.Journal of advanced research · 2025Article
- Identifying Biomarkers for Atherosclerosis via Gene Expression and Biological Networking.Current cardiology reviews · 2025Review
- LC-MS-based quantitation of proteomic changes induced by Norcantharidin in MTB-Treated macrophages.Proteome science · 2024Article
- Vav family exchange factors: Potential regulator in atherosclerosis.Biochemistry and biophysics reports · 2024Review
- Modification macrophage to foam cells in atherosclerosis disease: some factors stimulate or inhibit this process.Journal of diabetes and metabolic disorders · 2024Review
- Article
- Alveolar macrophage metabolic programming via a C-type lectin receptor protects against lipo-toxicity and cell death.Nature communications · 2022Article
- TRPM2 deficiency in mice protects against atherosclerosis by inhibiting TRPM2-CD36 inflammatory axis in macrophages.Nature cardiovascular research · 2022Article
- The computational analyses, molecular dynamics of fatty-acid transport mechanism to the CD36 receptor.Scientific reports · 2021Article
- Article
- miR-155-5p predictive role to decelerate foam cell atherosclerosis through CD36, VAV3, and SOCS1 pathway.Non-coding RNA research · 2021Article
- Siglec-E retards atherosclerosis by inhibiting CD36-mediated foam cell formation.Journal of biomedical science · 2021Article
- CD36 facilitates fatty acid uptake by dynamic palmitoylation-regulated endocytosis.Nature communications · 2020Article
- Lipoprotein receptor signalling in atherosclerosis.Cardiovascular research · 2020Review
- Role of macrophage TRPV4 in inflammation.Laboratory investigation; a journal of technical methods and pathology · 2020Review
- Lipoprotein(a) the Insurgent: A New Insight into the Structure, Function, Metabolism, Pathogenicity, and Medications Affecting Lipoprotein(a) Molecule.Journal of lipids · 2020Review
- CaJournal of clinical medicine · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Atherosclerosis, a chronic inflammatory disease, results in part from the accumulation of modified lipoproteins in the arterial wall and formation of lipid-laden macrophages, known as "foam cells." Recently, we reported that CD36, a scavenger receptor, contributes to activation of Vav-family guanine nucleotide exchange factors by oxidatively modified LDL in macrophages. We also discovered that CD36-dependent uptake of oxidized LDL (oxLDL) in vitro and foam cell formation in vitro and in vivo was significantly reduced in macrophages deficient of Vav proteins. The goal of the present study was to identify the mechanisms by which Vav proteins regulate CD36-dependent foam cell formation. We now show that a Vav-dynamin signaling axis plays a critical role in generating calcium signals in mouse macrophages exposed to CD36-specific oxidized phospholipid ligands. Chelation of intracellular Ca(2+) or inhibition of phospholipase C-γ (PLC-γ) inhibited Vav activation (85 and 70%, respectively, compared with vehicle control) and reduced foam cell formation (approximately 75%). Knockdown of expression by siRNA or inhibition of GTPase activity of dynamin 2, a Vav-interacting protein involved in endocytic vesicle fission, significantly blocked oxLDL uptake and inhibited foam cell formation. Immunofluorescence microscopy studies showed that Vav1 and dynamin 2 colocalized with internalized oxLDL in macrophages and that activation and mobilization of dynamin 2 by oxLDL was impaired in vav null cells. These studies identified previously unknown components of the CD36 signaling pathway, demonstrating that Vav proteins regulate oxLDL uptake and foam cell formation via calcium- and dynamin 2-dependent processes and thus represent novel therapeutic targets for atherosclerosis.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.