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  4. 氧化低密度脂蛋白誘發動脈粥狀硬化之致病機轉─內皮細胞氧化低密度脂蛋白受體LOX-1之訊息傳遞機制(3/3)
 
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氧化低密度脂蛋白誘發動脈粥狀硬化之致病機轉─內皮細胞氧化低密度脂蛋白受體LOX-1之訊息傳遞機制(3/3)

Other Title
Oxidized LDL signaling through the endothelial receptor- LOX-1 (3/3)
Date Issued
2002
Date
2002
Author(s)
李啟明
DOI
902320B002162M52
URI
http://ntur.lib.ntu.edu.tw//handle/246246/29783
Abstract
Oxidative modification of low-density lipoprotein (ox-LDL) is crucial in the pathogenesis of endothelial dysfunction, which is a major characteristic of atherosclerosis. Similar to that of macrophage, vascular endothelial cells can internalize ox-LDL. The recognition and uptake of ox-LDL in endothelial cells is different from that of macrophage in that it is mediated by LOX-1, a C-type lectin-like scavenger receptor. To date, the physiological effects of LOX-1 on protein activities and gene expression levels after it binds ox-LDL and internalizes into endothelial cells are still unclear. Our aim for this project was to investigate the molecular mechanism of endothelial cell dysfunction caused by ox-LDL. We first did yeast two-hybrid screen using the N-terminal domain of LOX-1 (LOX-1N) as the bait. Fifteen genes whose protein products interact with LOX-1N were cloned from a human heart cDNA library. Furthermore, we did microarray analysis and found in HUVEC cells 39 genes whose expression levels were changed after ox-LDL stimulation. Identification of these genes will help us understand the molecular effect of ox-LDL on endothelial cell function and discover new drugs for the treatments of atherosclerosis.
Subjects
ox-LDL
endothelial dysfunction
atherosclerosis
LOX-1
Publisher
臺北市:國立臺灣大學醫學院內科
Type
report
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902320B002162M52.pdf

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