Document Detail


Cutting edge: TNF-alpha-converting enzyme (TACE/ADAM17) inactivation in mouse myeloid cells prevents lethality from endotoxin shock.
MedLine Citation:
PMID:  17709479     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
TNF-alpha, a potent proinflammatory cytokine, is synthesized as a membrane-anchored precursor and proteolytically released from cells. Soluble TNF is the primary mediator of pathologies such as rheumatoid arthritis, Crohn's disease, and endotoxin shock. The TNF-alpha converting enzyme (TACE), a disintegrin and metalloprotease 17 (ADAM17), has emerged as the best candidate TNF sheddase, but other proteinases can also release TNF. Because TACE-deficient mice die shortly after birth, we generated conditional TACE-deficient mice to address whether TACE is the relevant sheddase for TNF in adult mice. In this study, we report that TACE inactivation in myeloid cells or temporal inactivation at 6 wk offers strong protection from endotoxin shock lethality in mice by preventing increased TNF serum levels. These findings corroborate that TACE is the major endotoxin-stimulated TNF sheddase in mouse myeloid cells in vivo, thereby further validating TACE as a principal target for the treatment of TNF-dependent pathologies.
Authors:
Keisuke Horiuchi; Tokuhiro Kimura; Takeshi Miyamoto; Hironari Takaishi; Yasunori Okada; Yoshiaki Toyama; Carl P Blobel
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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:  Journal of immunology (Baltimore, Md. : 1950)     Volume:  179     ISSN:  0022-1767     ISO Abbreviation:  J. Immunol.     Publication Date:  2007 Sep 
Date Detail:
Created Date:  2007-08-21     Completed Date:  2007-11-20     Revised Date:  2011-09-22    
Medline Journal Info:
Nlm Unique ID:  2985117R     Medline TA:  J Immunol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  2686-9     Citation Subset:  AIM; IM    
Affiliation:
Arthritis and Tissue Degeneration Program, Hospital for Special Surgery, Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.
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MeSH Terms
Descriptor/Qualifier:
ADAM Proteins / antagonists & inhibitors*,  genetics
Animals
GTP-Binding Proteins / genetics
Integrases / genetics
Mice
Mice, Mutant Strains
Myeloid Cells / enzymology*
Shock, Septic / enzymology,  prevention & control*
Grant Support
ID/Acronym/Agency:
R01 GM 64750/GM/NIGMS NIH HHS; R01 GM064750-09/GM/NIGMS NIH HHS
Chemical
Reg. No./Substance:
0/myxovirus resistance proteins; EC 2.7.7.-/Cre recombinase; EC 2.7.7.-/Integrases; EC 3.4.24.-/ADAM Proteins; EC 3.4.24.-/tumor necrosis factor-alpha convertase; EC 3.6.1.-/GTP-Binding Proteins

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


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