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• W2110284750 endingPage "362" @default.
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• W2110284750 abstract "Aims Electronegative LDL (LDL(−)), a minor modified LDL present in the circulation, induces cytokine release in monocytes. We aimed to determine the role of the receptor CD14 and toll-like receptors 2 and 4 (TLR2, TLR4) in the inflammatory action promoted by LDL(−) in human monocytes. Methods and results Monocytes were preincubated with antibodies to neutralize CD14, TLR2 and TLR4. The release of monocyte chemoattractant protein 1 (MCP1), and interleukin 6 and 10 (IL6 and IL10) promoted by LDL(−) was inhibited 70–80% by antiCD14 and antiTLR4, and 15–25% by antiTLR2. The involvement of CD14 and TLR4 was confirmed by gene silencing experiments. The human monocytic THP1 cell line overexpressing CD14 released more cytokines in response to LDL(−) than the same THP1 cell line without expressing CD14. VIPER, a specific inhibitor of the TLR4 signaling pathway, blocked 75–90% the cytokine release promoted by LDL(−). Cell binding experiments showed that monocytes preincubated with neutralizing antibodies presented lesser LDL(−) binding than non-preincubated monocytes The inhibitory capacity was antiCD14>antiTLR4>>antiTLR2. Cell-free experiments performed in CD14-coated microtiter wells confirmed that CD14 was involved in LDL(−) binding. When LDL(−) and lipopolysaccharide (LPS) were added simultaneously to monocytes, cytokine release was similar to that promoted by LDL(−) alone. Binding experiments showed that LDL(−) and LPS competed for binding to monocytes and to CD14 coated-wells. Conclusions CD14 and TLR4 mediate cytokine release induced by LDL(−) in human monocytes. The cross-competition between LPS and LDL(−) for the same receptors could be a counteracting action of LDL(−) in inflammatory situations." @default.
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• W2110284750 date "2013-08-01" @default.
• W2110284750 modified "2023-09-27" @default.
• W2110284750 title "CD14 and TLR4 mediate cytokine release promoted by electronegative LDL in monocytes" @default.
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• W2110284750 doi "https://doi.org/10.1016/j.atherosclerosis.2013.05.011" @default.
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