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dc.contributor.author Rock, JR
dc.contributor.author Randell, SH
dc.contributor.author Hogan, BL
dc.coverage.spatial England
dc.date.accessioned 2011-06-21T17:27:35Z
dc.date.issued 2010-09
dc.identifier http://www.ncbi.nlm.nih.gov/pubmed/20699479
dc.identifier dmm.006031
dc.identifier.citation Dis Model Mech, 2010, 3 (9-10), pp. 545 - 556
dc.identifier.uri http://hdl.handle.net/10161/4184
dc.description.abstract The small airways of the human lung undergo pathological changes in pulmonary disorders, such as chronic obstructive pulmonary disease (COPD), asthma, bronchiolitis obliterans and cystic fibrosis. These clinical problems impose huge personal and societal healthcare burdens. The changes, termed 'pathological airway remodeling', affect the epithelium, the underlying mesenchyme and the reciprocal trophic interactions that occur between these tissues. Most of the normal human airway is lined by a pseudostratified epithelium of ciliated cells, secretory cells and 6-30% basal cells, the proportion of which varies along the proximal-distal axis. Epithelial abnormalities range from hypoplasia (failure to differentiate) to basal- and goblet-cell hyperplasia, squamous- and goblet-cell metaplasia, dysplasia and malignant transformation. Mesenchymal alterations include thickening of the basal lamina, smooth muscle hyperplasia, fibrosis and inflammatory cell accumulation. Paradoxically, given the prevalence and importance of airway remodeling in lung disease, its etiology is poorly understood. This is due, in part, to a lack of basic knowledge of the mechanisms that regulate the differentiation, maintenance and repair of the airway epithelium. Specifically, little is known about the proliferation and differentiation of basal cells, a multipotent stem cell population of the pseudostratified airway epithelium. This Perspective summarizes what we know, and what we need to know, about airway basal cells to evaluate their contributions to normal and abnormal airway remodeling. We contend that exploiting well-described model systems using both human airway epithelial cells and the pseudostratified epithelium of the genetically tractable mouse trachea will enable crucial discoveries regarding the pathogenesis of airway disease.
dc.format.extent 545 - 556
dc.language ENG
dc.language.iso en_US en_US
dc.relation.ispartof Dis Model Mech
dc.relation.isversionof 10.1242/dmm.006031
dc.subject Airway Remodeling
dc.subject Animals
dc.subject Epithelium
dc.subject Homeostasis
dc.subject Humans
dc.subject Respiratory System
dc.subject Respiratory Tract Diseases
dc.subject Stem Cells
dc.title Airway basal stem cells: a perspective on their roles in epithelial homeostasis and remodeling.
dc.title.alternative en_US
dc.type Journal Article
dc.description.version Version of Record en_US
duke.date.pubdate 2010-10-sep en_US
duke.description.endpage 556 en_US
duke.description.issue 10-Sep en_US
duke.description.startpage 545 en_US
duke.description.volume 3 en_US
dc.relation.journal Disease Models & Mechanisms en_US
pubs.author-url http://www.ncbi.nlm.nih.gov/pubmed/20699479
pubs.issue 9-10
pubs.organisational-group /Duke
pubs.organisational-group /Duke/School of Medicine
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments
pubs.organisational-group /Duke/School of Medicine/Basic Science Departments/Cell Biology
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments
pubs.organisational-group /Duke/School of Medicine/Clinical Science Departments/Pediatrics
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers
pubs.organisational-group /Duke/School of Medicine/Institutes and Centers/Duke Cancer Institute
pubs.publication-status Published
pubs.volume 3
dc.identifier.eissn 1754-8411

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