Document Detail


Inhibition of interleukin 1beta converting enzyme family proteases reduces ischemic and excitotoxic neuronal damage.
MedLine Citation:
PMID:  9050895     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The interleukin 1beta converting enzyme (ICE) family plays a pivotal role in programmed cell death and has been implicated in stroke and neurodegenerative diseases. During reperfusion after filamentous middle cerebral artery occlusion, ICE-like cleavage products and tissue immunoreactive interleukin 1beta (IL-1beta) levels increased in ischemic mouse brain. Ischemic injury decreased after intracerebroventricular injections of ICE-like protease inhibitors, N-benzyloxycarbonyl-Val-Ala-Asp-fluoromethylketone (z-VAD.FMK), acetyl-Tyr-Val-Ala-Asp-chloromethylketone, or a relatively selective inhibitor of CPP32-like caspases, N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone, but not a cathepsin B inhibitor, N-benzyloxycarbonyl-Phe-Ala-fluoromethylketone. z-VAD.FMK decreased ICE-like cleavage products and tissue immunoreactive IL-1beta levels in ischemic mouse brain and reduced tissue damage when administered to rats as well. Only z-VAD.FMK and acetyl-Tyr-Val-Ala-Asp-chloromethylketone reduced brain swelling, and N-benzyloxycarbonyl-Asp-Glu-Val-Asp-fluoromethylketone did not attenuate the ischemia-induced increase in tissue IL-1beta levels. The three cysteine protease inhibitors significantly improved behavioral deficits, thereby showing that functional recovery of ischemic neuronal tissue can follow blockade of enzymes associated with apoptotic cell death. Finally, we examined the effect of z-VAD.FMK on excitotoxicity and found that it protected against alpha-amino-3-hydroxy-5-methyl-4-isoxazole propionate-induced or to a lesser extent N-methyl-D-aspartate-induced excitotoxic brain damage. Thus, ICE-like and CPP32-like caspases contribute to mechanisms of cell death in ischemic and excitotoxic brain injury and provide therapeutic targets for stroke and neurodegenerative brain damage.
Authors:
H Hara; R M Friedlander; V Gagliardini; C Ayata; K Fink; Z Huang; M Shimizu-Sasamata; J Yuan; M A Moskowitz
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Proceedings of the National Academy of Sciences of the United States of America     Volume:  94     ISSN:  0027-8424     ISO Abbreviation:  Proc. Natl. Acad. Sci. U.S.A.     Publication Date:  1997 Mar 
Date Detail:
Created Date:  1997-04-07     Completed Date:  1997-04-07     Revised Date:  2009-11-18    
Medline Journal Info:
Nlm Unique ID:  7505876     Medline TA:  Proc Natl Acad Sci U S A     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  2007-12     Citation Subset:  IM    
Affiliation:
Department of Surgery and Neurology, Massachusetts General Hospital, Harvard Medical School, Charlestown 02129, USA.
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MeSH Terms
Descriptor/Qualifier:
Animals
Blotting, Western
Brain / drug effects,  metabolism
Brain Ischemia / drug therapy*,  enzymology
Caspase 1
Caspase 3
Caspases*
Cathepsin B / antagonists & inhibitors
Cerebrovascular Disorders / drug therapy
Cysteine Endopeptidases / metabolism*
Cysteine Proteinase Inhibitors / pharmacology*
Gene Expression / genetics
Interleukin-1 / metabolism
Male
Mice
Neurons / drug effects*,  metabolism
Neurotoxins / pharmacology*
Rats
Rats, Sprague-Dawley
Receptors, Glutamate / metabolism
Reperfusion
Chemical
Reg. No./Substance:
0/Cysteine Proteinase Inhibitors; 0/Interleukin-1; 0/Neurotoxins; 0/Receptors, Glutamate; EC 3.4.22.-/Casp3 protein, mouse; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases; EC 3.4.22.-/Cysteine Endopeptidases; EC 3.4.22.1/Cathepsin B; EC 3.4.22.36/Caspase 1
Comments/Corrections

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


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