Microarray analysis of nicotine-induced changes in gene expression in endothelial cells
Microarray analysis of nicotine-induced changes in gene expression in endothelial cells
Cigarette smoking causes vascular endothelial dysfunction and is a major risk factor for cardiovascular diseases. Nicotine, a major constituent of cigarette smoke, has been shown to alter gene expression in endothelial cells; however, the regulatory pathways involved remain to be defined. We hypothesized that there might be distinct pathways that could be identified by systematic transcriptome analysis. Using the cDNA microarray approach, we ascertained the expression of over 4,000 genes in human coronary artery endothelial cells and identified a number of nicotine-modulated genes encoding a protein involving in signal transduction or transcriptional regulation. Among these were phosphatidylinositol phosphate kinase and diacylglycerol kinase, which are regulators of the inositol phospholipid pathway. Changes were also detected for transcription factors cAMP response element binding protein and nuclear factor-B, of which the activities of both have been previously shown to be altered in nicotine-stimulated cells. The data from this study are relevant to understanding the mechanisms underlying the pathophysiological effect of nicotine and smoking, particularly on endothelial function and pathogenesis of atherosclerosis.
microarray, inositol phospholipid pathway, camp response element binding protein, nuclear factor-b
187-192
Zhang, Shaoli
731ca399-f117-4aff-8d1d-36e59c919539
Day, Ian N.M.
b749b30a-1f4c-40eb-af0e-a50427388b39
Ye, Shu
132b6474-1927-4f93-80db-2c620a31c1ab
February 2001
Zhang, Shaoli
731ca399-f117-4aff-8d1d-36e59c919539
Day, Ian N.M.
b749b30a-1f4c-40eb-af0e-a50427388b39
Ye, Shu
132b6474-1927-4f93-80db-2c620a31c1ab
Zhang, Shaoli, Day, Ian N.M. and Ye, Shu
(2001)
Microarray analysis of nicotine-induced changes in gene expression in endothelial cells.
Physiological Genomics, 5 (4), .
Abstract
Cigarette smoking causes vascular endothelial dysfunction and is a major risk factor for cardiovascular diseases. Nicotine, a major constituent of cigarette smoke, has been shown to alter gene expression in endothelial cells; however, the regulatory pathways involved remain to be defined. We hypothesized that there might be distinct pathways that could be identified by systematic transcriptome analysis. Using the cDNA microarray approach, we ascertained the expression of over 4,000 genes in human coronary artery endothelial cells and identified a number of nicotine-modulated genes encoding a protein involving in signal transduction or transcriptional regulation. Among these were phosphatidylinositol phosphate kinase and diacylglycerol kinase, which are regulators of the inositol phospholipid pathway. Changes were also detected for transcription factors cAMP response element binding protein and nuclear factor-B, of which the activities of both have been previously shown to be altered in nicotine-stimulated cells. The data from this study are relevant to understanding the mechanisms underlying the pathophysiological effect of nicotine and smoking, particularly on endothelial function and pathogenesis of atherosclerosis.
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Published date: February 2001
Keywords:
microarray, inositol phospholipid pathway, camp response element binding protein, nuclear factor-b
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Local EPrints ID: 25061
URI: http://eprints.soton.ac.uk/id/eprint/25061
ISSN: 1094-8341
PURE UUID: 3e18392b-cad0-4dc9-82c0-24165b058a94
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Date deposited: 06 Apr 2006
Last modified: 22 Jul 2022 20:30
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Contributors
Author:
Shaoli Zhang
Author:
Ian N.M. Day
Author:
Shu Ye
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