Abstract
GPCR-mediated receptor transactivation of EGFR, is one of the effector mechanisms by which GPCR ligands, such as Ang II, thrombin and ET -1, catecholamine, SII-angiotensin, PAF, and uPA that are released at the arterial injury sites, can potentiate intimal hyperplasia. The process of EGFR transactivation can be cognate ligand-dependent or inde-pendent. In cognate ligand-dependent transactivation, ligand-bound GPCR results in the activation of metalloproteases, which sheds membrane tethered growth factor that binds to EGFR on an extracellular ligand-binding domain causing its transactivation. Whereas, in cognate ligand independent transactivation, ligand bound GPCR activates EGFR intracellularly via second messenger system. The mechanism of EGFR transactivation depends on cell type, GPCR ligand and the type of GPCR. In this review article, such cross-talks are critically discussed. The EGFR transactivation generates mitogenic signals leading to various pathological conditions. The goal of this review article is to identify potential targets for therapeutic intervention in clinical conditions related to intimal hyperplasia in cardiovascular system.
| Original language | English |
|---|---|
| Pages (from-to) | 190-201 |
| Number of pages | 12 |
| Journal | Current Vascular Pharmacology |
| Volume | 12 |
| Issue number | 2 |
| State | Published - Jan 1 2014 |
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All Science Journal Classification (ASJC) codes
- Cardiology and Cardiovascular Medicine
- Pharmacology
- Medicine(all)
Cite this
Transactivation of EGFR by G protein-coupled receptor in the pathophysiology of intimal hyperplasia. / Sur, Swastika; Agrawal, Devendra K.
In: Current Vascular Pharmacology, Vol. 12, No. 2, 01.01.2014, p. 190-201.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Transactivation of EGFR by G protein-coupled receptor in the pathophysiology of intimal hyperplasia
AU - Sur, Swastika
AU - Agrawal, Devendra K.
PY - 2014/1/1
Y1 - 2014/1/1
N2 - GPCR-mediated receptor transactivation of EGFR, is one of the effector mechanisms by which GPCR ligands, such as Ang II, thrombin and ET -1, catecholamine, SII-angiotensin, PAF, and uPA that are released at the arterial injury sites, can potentiate intimal hyperplasia. The process of EGFR transactivation can be cognate ligand-dependent or inde-pendent. In cognate ligand-dependent transactivation, ligand-bound GPCR results in the activation of metalloproteases, which sheds membrane tethered growth factor that binds to EGFR on an extracellular ligand-binding domain causing its transactivation. Whereas, in cognate ligand independent transactivation, ligand bound GPCR activates EGFR intracellularly via second messenger system. The mechanism of EGFR transactivation depends on cell type, GPCR ligand and the type of GPCR. In this review article, such cross-talks are critically discussed. The EGFR transactivation generates mitogenic signals leading to various pathological conditions. The goal of this review article is to identify potential targets for therapeutic intervention in clinical conditions related to intimal hyperplasia in cardiovascular system.
AB - GPCR-mediated receptor transactivation of EGFR, is one of the effector mechanisms by which GPCR ligands, such as Ang II, thrombin and ET -1, catecholamine, SII-angiotensin, PAF, and uPA that are released at the arterial injury sites, can potentiate intimal hyperplasia. The process of EGFR transactivation can be cognate ligand-dependent or inde-pendent. In cognate ligand-dependent transactivation, ligand-bound GPCR results in the activation of metalloproteases, which sheds membrane tethered growth factor that binds to EGFR on an extracellular ligand-binding domain causing its transactivation. Whereas, in cognate ligand independent transactivation, ligand bound GPCR activates EGFR intracellularly via second messenger system. The mechanism of EGFR transactivation depends on cell type, GPCR ligand and the type of GPCR. In this review article, such cross-talks are critically discussed. The EGFR transactivation generates mitogenic signals leading to various pathological conditions. The goal of this review article is to identify potential targets for therapeutic intervention in clinical conditions related to intimal hyperplasia in cardiovascular system.
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M3 - Article
C2 - 24568153
AN - SCOPUS:84900327239
VL - 12
SP - 190
EP - 201
JO - Current Vascular Pharmacology
JF - Current Vascular Pharmacology
SN - 1570-1611
IS - 2
ER -