ArticleBMC biochemistry2013
TNFa alter cholesterol metabolism in human macrophages via PKC-θ-dependent pathway.
Article in BMC biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Inflammation and immunomodulatory therapies influence the relationship between ATP-binding cassette A1 membrane transporter-mediated cholesterol efflux capacity and coronary atherosclerosis in rheumatoid arthritis.Journal of translational autoimmunity · 2023Article
- Mycobacterium tuberculosis/Mycobacterium bovis triggered different variations in lipid composition of Bovine Alveolar Macrophages.Scientific reports · 2022Article
- Hoodwinking the Big-Eater to Prosper: The Salmonella-Macrophage Paradigm.Journal of innate immunity · 2019Review
- Protein Kinase Cθ Via Activating Transcription Factor 2-Mediated CD36 Expression and Foam Cell Formation of Ly6CCirculation · 2018Article
- Modified LDL Particles Activate Inflammatory Pathways in Monocyte-derived Macrophages: Transcriptome Analysis.Current pharmaceutical design · 2018Article
- IL-32 promoter SNP rs4786370 predisposes to modified lipoprotein profiles in patients with rheumatoid arthritis.Scientific reports · 2017Article
- Role of PKCtheta in macrophage-mediated immune response to Salmonella typhimurium infection in mice.Cell communication and signaling : CCS · 2016Article
- Caveolae and Caveolin-1 Integrate Reverse Cholesterol Transport and Inflammation in Atherosclerosis.International journal of molecular sciences · 2016Review
- Low levels of CD36 in peripheral blood monocytes in subclinical atherosclerosis in rheumatoid arthritis: a cross-sectional study in a Mexican population.BioMed research international · 2014Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundStudies have shown that inflammation promoted atherosclerotic progression; however, it remains unclear whether inflammation promoted atherosclerotic progression properties by altering cholesterol metabolism in human macrophages. In the present study, we evaluated a potential mechanism of inflammation on atherogenic effects. We evaluated the ability of TNFa to affect Reverse cholesterol transport (RCT) and cholesterol uptake and its mechanism(s) of action in human macrophages.
resultsWe initially determined the potential effects of TNFa on cholesterol efflux in the human macrophages. We also determined alterations in mRNA and protein levels of ABCA1, ABCG1, LXRa, CD-36, SR-A in human macrophages using quantitative real-time polymerase chain reaction (PCR) and Western immunoblot analyses. The cholesterol efflux rate and protein expression of ABCA1, ABCG1, LXRa, CD-36, SR-A were quantified in human macrophages under PKC-θ inhibition using PKC-θ siRNA. Our results showed that TNFa inhibited the rate of cholesterol efflux and down-regulation the expression levels of ABCA1, ABCG1 and LXRa and up-regulation the expression levels of CD-36, SR-A in human macrophages; PKC-θ inhibition by PKC-θ siRNA attenuated the effect of TNFa on ABCA1, ABCG1, LXRa, SR-A, CD-36 expression.
conclusionsOur results suggest TNFa alter cholesterol metabolism in human macrophages through the inhibition of Reverse cholesterol transport and enhancing cholesterol uptake via PKC-θ-dependent pathway, implicating a potential mechanism of inflammation on atherogenic effects.
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