Journal
CANADIAN JOURNAL OF PHYSIOLOGY AND PHARMACOLOGY
Volume 93, Issue 3, Pages 171-176Publisher
CANADIAN SCIENCE PUBLISHING, NRC RESEARCH PRESS
DOI: 10.1139/cjpp-2014-0417
Keywords
asthma; COPD; AHR
Categories
Funding
- Canadian Institute of Health Research (CIHR)
- Canada Research Chair Program
- Canada Foundation for Innovation
- Manitoba Institute of Child Health (MICH)
- CIHR-Banting & Best Canada Graduate Scholarship
- CIHR-National Training Program in Allergy Asthma
- University of Manitoba Fellowship
- CIHR-GSK-CLA Fellowship
- Alberta Innovates Health Solutions early career development award
- Manitoba Health Research Council (MHRC)
- Canadian Respiratory Research Network (CRRN) Graduate Scholarship
- MHRC Graduate Scholarship
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Airway smooth muscle (ASM) contraction controls the airway caliber. Airway narrowing is exaggerated in obstructive lung diseases, such as asthma and chronic obstructive pulmonary disease (COPD). The mechanism by which ASM tone is dysregulated in disease is not clearly understood. Recent research on ion channels, particularly transient receptor potential cation channel, subfamily A, member 1 (TRPA1), is uncovering new understanding of altered airway function. TRPA1, a member of the TRP channel superfamily, is a chemo-sensitive cation channel that can be activated by a variety of external and internal stimuli, leading to the influx of Ca2+. Functional TRPA1 channels have been identified in neuronal and non-neuronal tissues of the lung, including ASM. In the airways, these channels can regulate the release of mediators that are markers of airway inflammation in asthma and COPD. For, example, TRPA1 controls cigarette-smoke-induced inflammatory mediator release and Ca2+ mobilization in vitro and in vivo, a response tied to disease pathology in COPD. Recent work has revealed that pharmacological or genetic inhibition of TRPA1 inhibits the allergen-induced airway inflammation in vitro and airway hyper-responsiveness (AHR) in vivo. Collectively, it appears that TRPA1 channels may be determinants of ASM contractility and local inflammation control, positioning them as part of novel mechanisms that control (patho) physiological function of airways and ASM.
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