GPCRs and arrestins in airways: implications for asthma.
Publication/Presentation Date
1-1-2014
Abstract
The obstructive lung disease asthma is treated by drugs that target, either directly or indirectly, G protein-coupled receptors (GPCRs). GPCRs coupled to Gq are the primary mediators of airway smooth muscle (ASM) contraction and increased airway resistance, whereas the Gs-coupled beta-2-adrenoceptor (β2AR) promotes pro-relaxant signaling in and relaxation of ASM resulting in greater airway patency and reversal of life-threatening bronchoconstriction. In addition, GPCR-mediated functions in other cell types, including airway epithelium and hematopoietic cells, are involved in the control of lung inflammation that causes most asthma. The capacity of arrestins to regulate GPCR signaling, via either control of GPCR desensitization/resensitization or G protein-independent signaling, renders arrestins an intriguing therapeutic target for asthma and other obstructive lung diseases. This review will focus on the potential role of arrestins in those GPCR-mediated airway cell functions that are dysregulated in asthma.
Volume
219
First Page
387
Last Page
403
ISSN
0171-2004
Published In/Presented At
Penn, R. B., Bond, R. A., & Walker, J. K. (2014). GPCRs and arrestins in airways: implications for asthma. Handbook of experimental pharmacology, 219, 387–403. https://doi.org/10.1007/978-3-642-41199-1_20
Disciplines
Business Administration, Management, and Operations | Health and Medical Administration | Management Sciences and Quantitative Methods
PubMedID
24292841
Department(s)
Administration and Leadership
Document Type
Article