Document Detail


alpha-1 antitrypsin inhibits caspase-3 activity, preventing lung endothelial cell apoptosis.
MedLine Citation:
PMID:  17003475     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
alpha-1 Antitrypsin (A1AT) is an abundant circulating serpin with a postulated function in the lung of potently inhibiting neutrophil-derived proteases. Emphysema attributable to A1AT deficiency led to the concept that a protease/anti-protease imbalance mediates cigarette smoke-induced emphysema. We hypothesized that A1AT has other pathobiological relevant functions in addition to elastase inhibition. We demonstrate a direct prosurvival effect of A1AT through inhibition of lung alveolar endothelial cell apoptosis. Primary pulmonary endothelial cells internalized human A1AT, which co-localized with and inhibited staurosporine-induced caspase-3 activation. In cell-free studies, native A1AT, but not conformers lacking an intact reactive center loop, inhibited the interaction of recombinant active caspase-3 with its specific substrate. Furthermore, overexpression of human A1AT via replication-deficient adeno-associated virus markedly attenuated alveolar wall destruction and oxidative stress caused by caspase-3 instillation in a mouse model of apoptosis-dependent emphysema. Our findings suggest that direct inhibition of active caspase-3 by A1AT may represent a novel anti-apoptotic mechanism relevant to disease processes characterized by excessive structural cell apoptosis, oxidative stress, and inflammation, such as pulmonary emphysema.
Authors:
Irina Petrache; Iwona Fijalkowska; Terry R Medler; Jarrett Skirball; Pedro Cruz; Lijie Zhen; Horia I Petrache; Terence R Flotte; Rubin M Tuder
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Publication Detail:
Type:  Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  The American journal of pathology     Volume:  169     ISSN:  0002-9440     ISO Abbreviation:  Am. J. Pathol.     Publication Date:  2006 Oct 
Date Detail:
Created Date:  2006-09-27     Completed Date:  2006-11-24     Revised Date:  2010-09-16    
Medline Journal Info:
Nlm Unique ID:  0370502     Medline TA:  Am J Pathol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1155-66     Citation Subset:  AIM; IM    
Affiliation:
Department of Medicine, The Johns Hopkins University School of Medicine, Baltimore, MD, USA. ipetrach@iupui.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis*
Capillaries / cytology,  drug effects,  enzymology
Caspase 3 / antagonists & inhibitors*,  metabolism*
Cell-Free System
Endothelial Cells / drug effects,  enzymology
Humans
Lung / blood supply,  cytology,  enzymology*
Lung Diseases / enzymology
Male
Mice
Mice, Inbred C57BL
alpha 1-Antitrypsin / metabolism*,  pharmacology*
Grant Support
ID/Acronym/Agency:
K08 HL04396-04/HL/NHLBI NIH HHS; P01-DK58327/DK/NIDDK NIH HHS; R01-HL69877/HL/NHLBI NIH HHS; R01HL66554/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/alpha 1-Antitrypsin; EC 3.4.22.-/Caspase 3
Comments/Corrections

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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