ArticleCytokine2010
Bioactive products generated by group V sPLA(2) hydrolysis of LDL activate macrophages to secrete pro-inflammatory cytokines.
Article in Cytokine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
10 citing papers in PubMed, 18 citations in OpenAlex.
- Omega-3 fatty acids reduce adipose tissue macrophages in human subjects with insulin resistance.Diabetes · 2013Trial
- Progress in the Cross-Organ Biomarker oxLDL in Promoting Pathological Neovascular Diseases.Antioxidants (Basel, Switzerland) · 2026Review
- Ceramide regulates interaction of Hsd17b4 with Pex5 and function of peroxisomes.Biochimica et biophysica acta. Molecular and cell biology of lipids · 2019Article
- Novel Role for Matrix Metalloproteinase 9 in Modulation of Cholesterol Metabolism.Journal of the American Heart Association · 2016Article
- Macrophages and Their Role in Atherosclerosis: Pathophysiology and Transcriptome Analysis.BioMed research international · 2016Review
- Anti-inflammatory effect of acetylpuerarin on eicosanoid signaling pathway in primary rat astrocytes.Journal of molecular neuroscience : MN · 2014Article
- Article
- Phospholipase A2 enzymes: physical structure, biological function, disease implication, chemical inhibition, and therapeutic intervention.Chemical reviews · 2011Review
- Phenotypic modulation of macrophages in response to plaque lipids.Current opinion in lipidology · 2011Review
- Secreted phospholipase A2, lipoprotein hydrolysis, and atherosclerosis: integration with lipidomics.Analytical and bioanalytical chemistry · 2011Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
objectivePrevious studies have established that hydrolysis of LDL by Group V secretory phospholipase A(2) (GV sPLA(2)) generates a modified particle capable of inducing macrophage foam cell formation. The aim of the present study was to determine whether GV sPLA(2)-hydrolyzed LDL (GV-LDL) produces pro-atherogenic effects in macrophages independent of cholesterol accumulation. METHODS AND
resultsJ-774 cells incubated with GV-LDL produced more TNF-alpha and IL-6 compared to cells incubated with control-LDL. Indirect immunofluorescence showed that GV-LDL but not control-LDL induced nuclear translocation of NFkappaB. Inhibitors of NFkappaB activation, effectively blocked cytokine production induced by GV-LDL. Control-LDL and GV-LDL were separated from albumin present in reaction mixtures by ultracentrifugation. The albumin fraction derived from GV-LDL contained 80% of the FFA generated and was more potent than the re-isolated GV-LDL in inducing pro-inflammatory cytokine secretion. Linoleic acid (18:2) and oleic acid (18:1) were the most abundant FFAs generated, whereas newly formed lyso-PCs contained 14:0 (myristic), 16:1 (palmitic), and 18:2 fatty acyl groups. Experiments with synthetic FFA showed that 18:1 induced J-774 cells to secrete TNF-alpha and IL-6.
conclusionsThese results indicate that in addition to promoting atherosclerotic lipid accumulation in macrophages, GV sPLA(2) hydrolysis of LDL leads to activation of NFkappaB, a key regulator of inflammation.
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Registered trials
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