Focal Adhesion Kinase Regulates Collagen I–Induced Airway Smooth Muscle Phenotype Switching
Abstract
Focal Adhesion Kinase Regulates Collagen I–Induced Airway Smooth Muscle Phenotype Switching var callbackToken='505F31853B61625'; var subCode='aspet_sub'; Skip to main page content HOME CURRENT ISSUE ARCHIVE FEEDBACK SUBSCRIPTIONS ALERTS HELP Keywords GO Advanced » Institution: DeepDyve Sign In as Member / Individual User Name Password Sign In Focal Adhesion Kinase Regulates Collagen I–Induced Airway Smooth Muscle Phenotype Switching Bart G. J. Dekkers , Anita I. R. Spanjer , Robert D. van der Schuyt , Willem Jan Kuik , Johan Zaagsma , and Herman Meurs Department of Molecular Pharmacology, University Centre for Pharmacy, and Groningen Research Institute for Asthma and COPD (GRIAC), University of Groningen, The Netherlands <h3>Address correspondence to:</h3> Bart G. J. Dekkers, Department of Molecular Pharmacology, University Centre for Pharmacy, University of Groningen, Antonius Deusinglaan 1, 9713 AV Groningen, The Netherlands. E-mail: b.g.j.dekkers@umcg.nl <h2>Abstract</h2> Increased extracellular matrix (ECM) deposition and airway smooth muscle (ASM) mass are major contributors to airway remodeling in asthma. Recently, we demonstrated that the ECM protein collagen I, which is increased surrounding asthmatic ASM, induces a proliferative, hypocontractile ASM phenotype. Little is known, however, about the signaling pathways involved. Using bovine tracheal smooth muscle, we investigated the role of focal adhesion kinase (FAK) and downstream