Transactivation of EGFR by G protein-coupled receptor in the pathophysiology of intimal hyperplasia

Swastika Sur, Devendra K. Agrawal

Research output: Contribution to journalArticle

14 Citations (Scopus)

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 languageEnglish
Pages (from-to)190-201
Number of pages12
JournalCurrent Vascular Pharmacology
Volume12
Issue number2
StatePublished - Jan 1 2014

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Tunica Intima
G-Protein-Coupled Receptors
Transcriptional Activation
Hyperplasia
Ligands
Angiotensins
Metalloproteases
Second Messenger Systems
Cardiovascular System
Thrombin
Catecholamines
Intercellular Signaling Peptides and Proteins
Membranes

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 journalArticle

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