Egr-1 is a Major Vascular Pathogenic Transcription Factor in Atherosclerosis and Restenosis

@article{Blaschke2004Egr1IA,
  title={Egr-1 is a Major Vascular Pathogenic Transcription Factor in Atherosclerosis and Restenosis},
  author={Florian Blaschke and Dennis Bruemmer and Ronald E. Law},
  journal={Reviews in Endocrine and Metabolic Disorders},
  year={2004},
  volume={5},
  pages={249-254}
}
The zinc finger transcription factor Egr-1 (early growth response factor-1), also known as nerve growth factorinduced-A (NGFI-A), zif268, Krox-24 and TIS8 was first identified by Sukhatme and colleagues [1]. It is the prototype of a family of zinc-finger transcription factors, that includes Egr-2, Egr-3 and Egr-4. Egr-1 is rapidly and transiently expressed in many different cell types in response to a variety of extracellular stimuli, including growth factors, cytokines and injurious stimuli [2… 

Regulation of the Early Growth Response Protein-1 in vascular smooth muscle cells

The role of Ca2+ signaling in Ang-IIinduced Egr-1 expression in VSMC is examined and the contribution of STIM-1 or Orai-1 is investigated as well as the associated signalling pathways.

Early Growth Response protein 1 (Egr-1) expression by Insulin-like growth factor 1 (IGF-1) involves MAPKs and PKB pathways

It is shown that IGF-1 stimulates the expression of Egr-1 through ERK1/2/JNK and PI3K/PKB and proposed that ROS generation plays an important role in this response.

Lysophosphatidic Acid Induces Early Growth Response Gene 1 Expression in Vascular Smooth Muscle Cells: CRE and SRE Mediate the Transcription

It is found that LPA markedly induces Egr-1 mRNA and protein in aortic smooth muscle cells (SMCs) and a novel role for CREB in mediating LPA-induced gene expression is established, implying that elevated LPA levels may exacerbate atheromatous lesions.

Early Growth Response Protein 1 Promotes Restenosis by Upregulating Intercellular Adhesion Molecule-1 in Vein Graft

Egr-1 may promote ECs proliferation and result in vein graft restenosis by upregulating the expression of ICAM-1, and could be a target for the prevention of restenotic after CABG surgery.

Transcription factor and kinase-mediated signaling in atherosclerosis and vascular injury

The focus of this review is to summarize the current understanding of a finite group of transcription factors and kinases involved in vascular injury and atherosclerosis, including nuclear factor-κB, early growth response factor-I (Egr-I), activator protein-I, hypoxia inducible factor- Iα (HIF-Iα), homeobox, and T cell factor/lymphoid enhancer factor (Tcf-Lef).

Insulin-like growth-factor-1-induced PKB signaling and Egr-1 expression is inhibited by curcumin in A-10 vascular smooth muscle cells.

Curcumin is a potent inhibitor of key components of the IGF-1-induced mitogenic and proliferative signaling system in VSMC, and it is suggested that curcumin-induced attenuation of these signaling components may constitute a potential mechanism for its vasculoprotective effects.

Attenuation of endothelin-1-induced PKB and ERK1/2 signaling, as well as Egr-1 expression, by curcumin in A-10 vascular smooth muscle cells.

Curcumin is a potent inhibitor of ET-1-induced mitogenic and proliferative signaling events in VSMC and the ability of curcumin to attenuate these events may contribute as a potential mechanism for its cardiovascular protective response.

Role of receptor and non-receptor protein tyrosine kinases in vasoactive peptide-induced signaling

This work investigated whether IGF-1R transactivation plays a similar role in ET-1 and Ang II-induced PKB phosphorylation and hypertrophic responses in VSMC.
...

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