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

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

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
Volume318
Issue number2
DOIs
Publication statusPublished - 2004 May 28

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Peroxisome Proliferator-Activated Receptors
Transcription Factor AP-1
Fenofibrate
Interleukin-8
Smooth Muscle Myocytes
Muscle
Chemical activation
Cells
Up-Regulation
MAP Kinase Kinase 4
Cell proliferation
Vascular Smooth Muscle
LDL Lipoproteins
Cardiovascular Diseases
Phosphotransferases
Cell Proliferation
Modulation
oxidized low density lipoprotein

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Biophysics
  • Molecular Biology

Cite this

Ryoo, Sungwoo ; Won, Misun ; Kim, Dong Uk ; Kim, Lila ; Han, Gyoonhee ; Park, Seung Kiel ; Mukaida, Naofumi ; Maeng, Piljae ; Yoo, Hyang Sook ; Hoe, Kwang Lae. / PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells. In: Biochemical and Biophysical Research Communications. 2004 ; Vol. 318, No. 2. pp. 329-334.
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PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells. / Ryoo, Sungwoo; Won, Misun; Kim, Dong Uk; Kim, Lila; Han, Gyoonhee; Park, Seung Kiel; Mukaida, Naofumi; Maeng, Piljae; Yoo, Hyang Sook; Hoe, Kwang Lae.

In: Biochemical and Biophysical Research Communications, Vol. 318, No. 2, 28.05.2004, p. 329-334.

Research output: Contribution to journalArticle

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AU - Ryoo, Sungwoo

AU - Won, Misun

AU - Kim, Dong Uk

AU - Kim, Lila

AU - Han, Gyoonhee

AU - Park, Seung Kiel

AU - Mukaida, Naofumi

AU - Maeng, Piljae

AU - Yoo, Hyang Sook

AU - Hoe, Kwang Lae

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N2 - 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.

AB - 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.

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