상세 정보

underline
Metadata Downloads : dc(xml) or Excel
Cited 0 time in scopus ci

Title 

Native LDL induces interleukin-8 expression via H2O2, p38 Kinase, and activator protein-1 in human aortic smooth muscle cells

Authors 

Sung Woo RyooDong Uk KimMi Sun WonKyung Sook ChungYoung Joo JangGoo Taeg OhSong Kyu ParkP J MaengHyang Sook YooKwang Lae Hoe

Publisher 

Oxford University Press (OUP)

Issue Date 

2004

Citation 

Cardiovascular Research, vol. 62, no. 1, pp. 185-193

Keywords 

atherosclerosisinterleukinslipoproteinsMAP kinasesmooth muscleimmunoglobulin enhancer binding proteininterleukin 8low density lipoproteinmitogen activated protein kinase 1protein

Abstract 

Background and objectives: Endothelial and monocytic cells appear to play a key role in the initiation and progression of atherosclerosis and restenosis via the upregulation of inflammatory cytokines and the formation of oxidized low-density lipoprotein (ox-LDL). However, the role of smooth muscle cells (SMCs) has been underestimated and is not well understood. It was investigated for the first time that native LDL stimulates human SMCs to secrete IL-8. The aim of this study was to investigate the signaling pathway involved in the upregulation of IL-8, induced by LDL in human aortic SMCs. Methods and results: LDL-induced IL-8 expression (mRNA and protein) is specific to SMCs and likely to be regulated at the transcription level in dose- and time-dependent manners, as judged by experiments with actinomycin D and ELISA. Although both p38 and ERK 1/2 MAPKs were activated by LDL, only p38 MAPK is responsible for the LDL effects, as evidenced by a complete blockade of IL-8 upregulation by SB203580. Pretreatment with catalase significantly decreased the extent of IL-8 upregulation, indicating that H2O2 is necessary for the LDL response. Activation of activator protein (AP)-1, but not nuclear factor (NF)-κB, by p38 or H2O2 appears to be necessary along with the concomitant upregulation of c-fos and c-JUN, as judged by electrophoretic mobility shift and luciferase reporter assays. Conclusions: These data demonstrated that LDL stimulates SMCs to induce IL-8 production in dose- and time-dependent manners at the transcription level and that the LDL signaling in hAoSMCs is conveyed via the generation of H2O 2, the phosphorylation of p38 MAPK, the activation of AP-1, and the participation of NF-κB.

ISSN 

0008-6363

Link 

http://dx.doi.org/10.1016/j.cardiores.2004.01.002

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


There are no files associated with this item.
qrcode

FusionCharts.
DSpace Software Coptright(c) 2010 MIT and Hewleft-Packard  /  KRIBB-REPOSITORY ( Email:jakim@kribb.re.kr)