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Title 

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

Authors 

Sung Woo RyooMi Sun WonDong Uk KimLila KimGyoon Hee HanS K ParkN MukaidaP J MaengHyang Sook YooKwang Lae Hoe

Publisher 

Elsevier

Issue Date 

2004

Citation 

Biochemical and Biophysical Research Communications, vol. 318, no. 2, pp. 329-334

Keywords 

AP-1fenofibrateinterleukin-8low-density lipoproteinPPARsmooth muscle cellinterleukin 8synaptophysintranscription factor AP 1antilipemic agent

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.

ISSN 

0006-291X

Link 

http://dx.doi.org/10.1016/j.bbrc.2004.04.031

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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