Evidence map›Paper›PMID 10712437›Full record

ArticleThe Journal of clinical investigation2000

High-level expression of Egr-1 and Egr-1-inducible genes in mouse and human atherosclerosis.

T A McCaffrey, C Fu, B Du, S Eksinar, K C Kent, H Bush, K Kreiger, T Rosengart, M I Cybulsky, E S Silverman and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of clinical investigation, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 87 papers.

0numbers the graph read from it
0cells of the map it votes in
87citing papers in PubMed
8.4field-weighted citation impact, top 1% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

87 citing papers in PubMed, 298 citations in OpenAlex.

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  14. S14G-humanin (HNG) protects retinal endothelial cells from UV-B-induced NLRP3 inflammation activation through inhibiting Egr-1.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2021
    Article
  15. Review
  16. Long Noncoding RNACirculation · 2021
    Article
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27 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

11 authors at 5 institutions in 2 countries.

T A McCaffreyDepartment of Medicine, Division of Hematology/Oncology, Weill Medical College of Cornell University, New York, New York 10021, USA. tamccaf@med.cornell.edu
C Fu
B Du
S Eksinar
K C Kent
H Bush
K Kreiger
T Rosengart
M I Cybulsky
E S Silverman
T Collins
Cornell University · USCenter for Vascular Biology Research · USBrigham and Women's Hospital · USHarvard University · USUniversity of Toronto · CA

Funding

NUCLEAR FACTOR KAPPA BETA AND THE INITIATION OF THE ATHEROSCLEROTIC LESIONP50HL056985 · NHLBI · BRIGHAM AND WOMEN'S HOSPITAL · PI GIMBRONE, MICHAEL A · 1997 to 2006
$14.1M
TGF-BETA 1 RECEPTORS IN RESTENOSIS AND AGINGR37AG012712 · NIA · GEORGE WASHINGTON UNIVERSITY · PI MCCAFFREY, TIMOTHY A. · 2001 to 2009
$2.9M
SCOR IN MOLECULAR MEDICINE AND ATHEROSCLEROSISP50HL056987 · NHLBI · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI CRYSTAL, RONALD G · 1997 to 2001
$2.4M
TRANSCRIPTIONAL REGULATION OF PDGF BY ENDOTHELIUMR37HL035716 · NHLBI · CHILDREN'S HOSPITAL BOSTON · PI COLLINS, TUCKER O · 1996 to 2005
$1.9M
TGF-B1 RECEPTORS IN RESTENOSIS AND AGINGR01AG012712 · NIA · WEILL MEDICAL COLLEGE OF CORNELL UNIV · PI MCCAFFREY, TIMOTHY A. · 1996 to 2000
$403k
NHLBI NIH HHS HL56985NHLBI NIH HHS HL56987NHLBI NIH HHS P50 HL056985NHLBI NIH HHS R37 HL035716NIA NIH HHS AG12712NIA NIH HHS R01 AG012712NIA NIH HHS R37 AG012712
6 · The paper itself

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-beta. 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 Egr-1-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.

Indexed as

Immediate-Early ProteinsAnimalsArteriosclerosisDiet, AtherogenicDNA-Binding ProteinsEarly Growth Response Protein 1Gene Expression RegulationHumansImmunohistochemistryMiceMice, KnockoutMuscle, Smooth, VascularReceptors, LDLRNA, MessengerTranscription FactorsDNA-Binding ProteinsEarly Growth Response Protein 1EGR1 protein, humanEgr1 protein, mouseImmediate-Early ProteinsReceptors, LDLRNA, MessengerTranscription Factors

Identifiers

PMID10712437
PMCPMC289183
OpenAlexW1993573575

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.