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- PPAR α activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells
- Sung Woo Ryoo; Mi Sun Won; Dong Uk Kim; Lila Kim; Gyoon Hee Han; S K Park; N Mukaida; P J Maeng; Hyang Sook Yoo; Kwang Lae Hoe
- Bibliographic Citation
- Biochemical and Biophysical Research Communications, vol. 318, no. 2, pp. 329-334
- Publication Year
- Native low density lipoprotein (n-LDL) is a major risk factor for cardiovascular diseases by inducing inflammatory processes and vascular smooth muscle cell proliferation in vessel cells. It has previously been reported that LDL enhances inflammatory reactions by the up-regulation of interleukin (IL)-8 via the activation of p38 kinase and activator protein (AP)-1 in human aortic smooth muscle cells (hAoSMCs). The findings of this study show, for the first time, that the peroxisome proliferator-activated receptor (PPARα) agonist, fenofibrate, completely abolishes the LDL-induced IL-8 up-regulation at the transcriptional level. Pretreatment of hAoSMCs with fenofibrate abolishes the effects of LDL on AP-1 activation without affecting nuclear factor (NF)-κB. In contrast, fenofibrate failed to modulate the activation state of p38 and JNK kinases or the levels of c-fos and phospho-Jun. These data suggest that AP-1 is likely to be located at the crossroads between LDL signaling and the regulation of IL-8 modulation by PPARα.
- AP-1; fenofibrate; interleukin-8; low-density lipoprotein; PPAR; smooth muscle cell
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- Division of Biomedical Research > Personalized Genomic Medicine Research Center > 1. Journal Articles
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
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