Document Detail


Cell death, remodeling, and repair in chronic obstructive pulmonary disease?
MedLine Citation:
PMID:  17065379     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Apoptotic cells can be detected in the parenchyma and airways of patients with chronic obstructive pulmonary disease (COPD) in greater numbers than seen in normal lungs or those from smokers without COPD. Implications include more apoptosis and/or decreased clearance of apoptotic cells. Both epithelial and endothelial cells become apoptotic. What role does the apoptosis play in the emphysema or small airway alterations seen in COPD? In simple terms, loss of cells by apoptosis would be expected to accompany, or perhaps initiate, the overall tissue destruction normally believed responsible. Indeed, direct induction of apoptosis in pulmonary endothelial or epithelial cells in rodents is accompanied by emphysematous changes. On the other hand, apoptotic cells are normally removed from tissues rapidly with minimal tissue response, to be followed by cell replacement to maintain homeostasis. The presence of detectable apoptotic cells, therefore, may imply defects in these clearance mechanisms, and, in keeping with this hypothesis, there is increasing evidence for such defects in patients with COPD. Mice with abnormalities in apoptotic cell removal also tend to develop spontaneous "emphysema." A reconciling hypothesis is that recognition of apoptotic cells not only leads to removal but also, normally, to signals for cell replacement. If this latter response is lacking in COPD-susceptible smokers, defects in normal alveolar or small airway repair could significantly contribute to the structural disruption. The concept puts emphasis on defective repair as well as initial injury (i.e., persistent alteration of dynamic tissue homeostasis, as a key contributor to COPD), with, it is hoped, additional approaches for mitigation.
Authors:
Peter M Henson; R William Vandivier; Ivor S Douglas
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't; Review    
Journal Detail:
Title:  Proceedings of the American Thoracic Society     Volume:  3     ISSN:  1546-3222     ISO Abbreviation:  Proc Am Thorac Soc     Publication Date:  2006 Nov 
Date Detail:
Created Date:  2006-10-26     Completed Date:  2007-01-23     Revised Date:  2013-06-07    
Medline Journal Info:
Nlm Unique ID:  101203596     Medline TA:  Proc Am Thorac Soc     Country:  United States    
Other Details:
Languages:  eng     Pagination:  713-7     Citation Subset:  IM    
Affiliation:
National Jewish Medical and Research Center, 1400 Jackson Street, Denver, CO 80206, USA. hensonp@njc.org
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis / physiology*
Bronchi / cytology*,  injuries
Disease Models, Animal
Emphysema / physiopathology
Homeostasis
Humans
Mice
Pulmonary Disease, Chronic Obstructive / physiopathology*
Regeneration / physiology*
Respiratory Mucosa / cytology*,  injuries
Grant Support
ID/Acronym/Agency:
GM61031/GM/NIGMS NIH HHS; HL070940/HL/NHLBI NIH HHS; HL072018/HL/NHLBI NIH HHS; HL68864/HL/NHLBI NIH HHS; HL81151/HL/NHLBI NIH HHS
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