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
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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