Transactivation of EGFR by G Protein-Coupled Receptor in the Pathophysiology of Intimal Hyperplasia

Title:Transactivation of EGFR by G Protein-Coupled Receptor in the Pathophysiology of Intimal Hyperplasia

Volume: 12 Issue: 2

Author(s): Swastika Sur and Devendra K. Agrawal

Affiliation:

Keywords: A disintegrin and metalloproteinases, cell proliferation, epidermal growth factor receptor, g-protein coupled receptor, intimal hyperplasia, matrix matalloproteinases, migration, transactivation.

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 independent. 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.

Cite this article as:

Sur Swastika and Agrawal K. Devendra, Transactivation of EGFR by G Protein-Coupled Receptor in the Pathophysiology of Intimal Hyperplasia, Current Vascular Pharmacology 2014; 12 (2) . https://dx.doi.org/10.2174/1570161112666140226123745