High-level expression of Egr-1 and Egr-1-inducible genes in mouse and human atherosclerosis
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Output type: Journal article
Author list: McCaffrey T., Fu C., Du B., Eksinar S., Kent K., Harry B., Kreiger K., Rosengart T., Cybulsky M., Silverman E., Collins T.
Publisher: American Society for Clinical Investigation
Publication year: 2000
Journal: Journal of Clinical Investigation (0021-9738)
Volume number: 105
Issue number: 5
Start page: 653
End page: 662
Number of pages: 10
ISSN: 0021-9738
eISSN: 1558-8238
URL: http://api.elsevier.com/content/abstract/scopus_id:0034060981
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Open access status: bronze
Full text URL: http://www.jci.org/articles/view/8592/files/pdf
Abstract
To understand the mRNA transcript profile in the human atherosclerotic lesion, RNA was prepared from the fibrous cap versus adjacent media of 13 patients undergoing carotid endarterectomy. cDNA expression arrays bearing 588 known genes indicated that lesions express unexpectedly high levels of the early growth response gene, Egr-1 (NGFI-A), a zinc-finger transcription factor that modulates a cluster of stress-responsive genes including PDGF and TGF-β. Expression of Egr-1 was an average of 5-fold higher in the lesion than in the adjacent media, a result confirmed by RT-PCR, and many Egr1- inducible genes were also strongly elevated in the lesion. Time-course analyses revealed that Egr-1 was not induced ex vivo. Immunocytochemistry indicated that Egr-1 was expressed prominently in the smooth muscle-actin positive cells, particularly in areas of macrophage infiltration, and in other cell types, including endothelial cells. Induction of atherosclerosis in LDL receptor-null mice by feeding them a high-fat diet resulted in a progressive increase in Egr-1 expression in the aorta. Thus, induction of Egr-1 by atherogenic factors may be a key step in coordinating the cellular events that result in vascular lesions.
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