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Biochem Biophys Res Commun. 2012 Aug 24;425(2):121-6. doi: 10.1016/j.bbrc.2012.07.011. Epub 2012 Jul 13.

Oxidized low-density lipoprotein induces secretion of interleukin-1β by macrophages via reactive oxygen species-dependent NLRP3 inflammasome activation.

Author information

1
Division of Vascular Surgery, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, PR China.

Abstract

Oxidized low-density lipoprotein (ox-LDL) is a critical mediator of atherogenesis. Macrophage uptake of ox-LDL and their subsequent development into foam cells is the principal event in atherosclerosis. Interleukin-1β (IL-1β), a prototypic multifunctional cytokine involved in inflammation, has an important effect on the pathogenesis and progression of atherosclerosis. Here we show that the phagocytosis of ox-LDL can induce human macrophages to secrete IL-1β by activating the NLRP3 inflammasome, and we further show that the activation of the NLRP3 inflammasome is dependent on the generation of reactive oxygen species and is related to the cathepsin B pathway. Furthermore, ox-LDL can upregulate the expression of the pro-IL-1β protein, thus priming IL-1β secretion. Therefore, our results suggest that the role of ox-LDL in atherosclerosis-related inflammation may involve the activation of the NLRP3 inflammasome.

PMID:
22796220
DOI:
10.1016/j.bbrc.2012.07.011
[Indexed for MEDLINE]

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