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 language | English |
|---|---|
| Pages (from-to) | 329-334 |
| Number of pages | 6 |
| Journal | Biochemical and Biophysical Research Communications |
| Volume | 318 |
| Issue number | 2 |
| DOIs | |
| Publication status | Published - 2004 May 28 |
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All Science Journal Classification (ASJC) codes
- Biochemistry
- Biophysics
- Molecular Biology
Cite this
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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 journal › Article
TY - JOUR
T1 - PPARα activation abolishes LDL-stimulated IL-8 production via AP-1 deactivation in human aortic smooth muscle cells
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
PY - 2004/5/28
Y1 - 2004/5/28
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.
UR - http://www.scopus.com/inward/record.url?scp=2142715921&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=2142715921&partnerID=8YFLogxK
U2 - 10.1016/j.bbrc.2004.04.031
DO - 10.1016/j.bbrc.2004.04.031
M3 - Article
VL - 318
SP - 329
EP - 334
JO - Biochemical and Biophysical Research Communications
JF - Biochemical and Biophysical Research Communications
SN - 0006-291X
IS - 2
ER -