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Involvement of the Early Growth Response Protein 1 in Vascular Pathophysiology: An Overview

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Title Involvement of the Early Growth Response Protein 1 in Vascular Pathophysiology: An Overview
 
Creator Cheyou, Estelle R Simo
Youreva, Viktoria
Srivastava, Ashok K
 
Subject Egr-1
Transcription
Vascular diseases
Signaling
Proliferation
MAP Kinase
 
Description 457-466
Hyperactivation of proliferative and growth promoting pathways underlies
the progression of vessel remodeling, leading to vascular dysfunction. An upregulation of early
growth response protein 1 (Egr-1), a zinc finger transcription factor has been
observed in several models of vascular diseases. In the vasculature, Egr-1
expression can be induced by multiple hormonal, metabolic and external stimuli,
such as growth factors, cytokines, reactive oxygen species, hyperglycaemia and stretch-induced
stress. The structure of the Egr-1 promoter allows both its auto-regulation and
its binding with several regulatory transcription cofactors like the serum
response factor and the cAMP response element binding protein. Pharmacological
and genetic studies have revealed the involvement of several signaling pathways
that contribute to the expression of Egr-1. Among them, the mitogen-activated
protein kinase pathway has emerged as a predominant signaling cascade that
regulates Egr-1 transcription in response to various stimuli. Moreover, targeted
deletion of Egr-1 by DNAzymes, antisense oligonucleotides or RNA interference
has also helped in defining the importance of Egr-1 in the pathophysiology of
vascular diseases. Neointimal formation and expression of genes directly linked
with proinflammatory processes have been demonstrated to be enhanced by Egr-1
expression and activity. This review provides an overview on the signaling
components implicated in Egr-1 expression and discusses its potential
involvement in vascular pathophysiology.


 
Date 2015-02-11T04:20:26Z
2015-02-11T04:20:26Z
2014-12
 
Type Article
 
Identifier 0975-0959 (Online); 0301-1208 (Print)
http://hdl.handle.net/123456789/30494
 
Language en_US
 
Rights CC Attribution-Noncommercial-No Derivative Works 2.5 India
 
Publisher NISCAIR-CSIR, India
 
Source IJBB Vol.51(6) [December 2014]