Document Detail


Caspase-3 activation in astrocytes following postnatal excitotoxic damage correlates with cytoskeletal remodeling but not with cell death or proliferation.
MedLine Citation:
PMID:  17487878     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Caspase-3 has classically been defined as the main executioner of programmed cell death. However, recent data supports the participation of this protease in non-apoptotic cellular events including cell proliferation, cell cycle regulation, and cellular differentiation. In this study, astroglial cleavage of caspase-3 was analyzed following excitotoxic damage in postnatal rats to determine if its presence is associated with apoptotic cell death, cell proliferation, or cytoskeletal remodeling. A well-characterized in vivo model of excitotoxicity was studied, where damage was induced by intracortical injection of N-methyl-D-asparate (NMDA) in postnatal day 9 rats. Our results demonstrate that cleaved caspase-3 was mainly observed in the nucleus of activated astrocytes in the lesioned hemisphere as early as 4 h postlesion and persisted until the glial scar was formed at 7-14 days, and it was not associated with TUNEL labeling. Caspase-3 enzymatic activity was detected at 10 h and 1 day postlesion in astrocytes, and co-localized with caspase-cleaved fragments of glial fibrillary acidic protein (CCP-GFAP). However, at longer survival times, when astroglial hypertrophy was observed, astroglial caspase-3 did not generally correlate with GFAP cleavage, but instead was associated with de novo expression of vimentin. Moreover, astroglial caspase-3 cleavage was not associated with BrdU incorporation. These results provide further evidence for a nontraditional role of caspases in cellular function that is independent of cell death and suggest that caspase activation is important for astroglial cytoskeleton remodeling following cellular injury.
Authors:
Laia Acarin; Sonia Villapol; Maryam Faiz; Troy T Rohn; Bernardo Castellano; Berta González
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Glia     Volume:  55     ISSN:  0894-1491     ISO Abbreviation:  Glia     Publication Date:  2007 Jul 
Date Detail:
Created Date:  2007-05-30     Completed Date:  2007-07-25     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  8806785     Medline TA:  Glia     Country:  United States    
Other Details:
Languages:  eng     Pagination:  954-65     Citation Subset:  IM    
Copyright Information:
(c) 2007 Wiley-Liss, Inc.
Affiliation:
Medical Histology, Department of Cell Biology, Physiology and Immunology, Faculty of Medicine and Institute of Neurosciences, Autonomous University of Barcelona, Spain. Laia.acarin@uab.es
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Astrocytes / drug effects,  enzymology*,  pathology
Brain / enzymology*,  pathology,  physiopathology
Brain Damage, Chronic / enzymology*,  physiopathology
Caspase 3 / metabolism*
Cell Death / drug effects,  physiology
Cell Proliferation / drug effects
Cell Size / drug effects
Cytoskeleton / drug effects,  enzymology*,  pathology
Enzyme Activation / drug effects,  physiology
Female
Glial Fibrillary Acidic Protein / metabolism
Gliosis / chemically induced*,  enzymology,  physiopathology
Intermediate Filaments / drug effects,  metabolism,  pathology
Male
N-Methylaspartate / metabolism,  toxicity
Nerve Degeneration / chemically induced,  enzymology,  physiopathology
Neurotoxins / metabolism,  toxicity
Rats
Rats, Long-Evans
Vimentin / metabolism
Chemical
Reg. No./Substance:
0/Glial Fibrillary Acidic Protein; 0/Neurotoxins; 0/Vimentin; 6384-92-5/N-Methylaspartate; EC 3.4.22.-/Caspase 3

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


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