| Caspase-3 activation in astrocytes following postnatal excitotoxic damage correlates with cytoskeletal remodeling but not with cell death or proliferation. | |
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MedLine Citation:
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PMID: 17487878 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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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. |
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Authors:
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Laia Acarin; Sonia Villapol; Maryam Faiz; Troy T Rohn; Bernardo Castellano; Berta González |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't |
Journal Detail:
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Title: Glia Volume: 55 ISSN: 0894-1491 ISO Abbreviation: Glia Publication Date: 2007 Jul |
Date Detail:
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Created Date: 2007-05-30 Completed Date: 2007-07-25 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 8806785 Medline TA: Glia Country: United States |
Other Details:
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Languages: eng Pagination: 954-65 Citation Subset: IM |
Copyright Information:
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(c) 2007 Wiley-Liss, Inc. |
Affiliation:
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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 |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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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:
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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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