화학공학소재연구정보센터
Biochemical and Biophysical Research Communications, Vol.335, No.2, 603-608, 2005
Very low-density lipoprotein induces interleukin-1 beta expression in macrophages
Elevated plasma level of very low-density lipoprotein (VLDL) is a risk factor for coronary heart disease. We investigated the effect of VLDL on expression of the pro-inflammatory cytokine interleukin-1 beta (IL-1 beta) in human peripheral blood monocyte-derived macrophages. IL-1 beta mRNA and protein expression was analysed by PCR and ELISA, respectively. Caspase activation was assessed by immunoblotting. Apart from potentiating lipopolysaccharide-induced secretion of IL-1 beta, VLDL alone induced secretion of IL-1 beta from human monocyte-derived macrophages. This effect was suppressed by an inhibitor of caspase-1, the protease which cleaves pro-IL-1 beta. VLDL treatment activated caspase-1, as indicated by increased levels of the caspase-1 p20 subunit. Furthermore, VLDL increased IL-1 beta mRNA expression, which was associated with activation of transcription factor AP-1. Inhibition of caspase-1 did not influence IL-1 beta mRNA expression. In conclusion, VLDL induces IL-1 beta mRNA expression, caspase-1 activation, and IL-1 beta release from macrophages, suggesting that VLDL can promote inflammation in atherosclerotic lesions. (c) 2005 Elsevier Inc. All rights reserved.