PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells

Sungwoo Ryoo, Misun Won, Dong Uk Kim, Lila Kim, Gyoonhee Han, Seung Kiel Park, Naofumi Mukaida, Piljae Maeng, Hyang Sook Yoo, Kwang Lae Hoe

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14 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)329-334
Number of pages6
JournalBiochemical and Biophysical Research Communications
Issue number2
Publication statusPublished - 2004 May 28

Bibliographical note

Funding Information:
This work was supported by the Molecular and Cellular BioDiscovery Research Program and 21st Century Frontier R&D Program from the Ministry of Science and Technology of Korea and by Korea Research Institute of Bioscience and Biotechnology. We thank Professor S.-W. Kwon at the Asan Medical Center for his help in the preparation of LDL.

All Science Journal Classification (ASJC) codes

  • Biophysics
  • Biochemistry
  • Molecular Biology
  • Cell Biology


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