| Concurrent assessment of calpain and caspase-3 activation after oxygen-glucose deprivation in primary septo-hippocampal cultures. | |
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MedLine Citation:
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PMID: 11702043 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The contributions of calpain and caspase-3 to apoptosis and necrosis after central nervous system (CNS) trauma are relatively unexplored. No study has examined concurrent activation of calpain and caspase-3 in necrotic or apoptotic cell death after any CNS insult. Experiments used a model of oxygen-glucose deprivation (OGD) in primary septo-hippocampal cultures and assessed cell viability, occurrence of apoptotic and necrotic cell death phenotypes, and protease activation. Immunoblots using an antibody detecting calpain and caspase-3 proteolysis of alpha-spectrin showed greater accumulation of calpain-mediated breakdown products (BDPs) compared with caspase-3-mediated BDPs. Administration of calpain and caspase-3 inhibitors confirmed that activation of these proteases contributed to cell death, as inferred by lactate dehydrogenase release. Oxygen-glucose deprivation resulted in expression of apoptotic and necrotic cell death phenotypes, especially in neurons. Immunocytochemical studies of calpain and caspase-3 activation in apoptotic cells indicated that these proteases are almost always concurrently activated during apoptosis. These data demonstrate that calpain and caspase-3 activation is associated with expression of apoptotic cell death phenotypes after OGD, and that calpain activation, in combination with caspase-3 activation, could contribute to the expression of apoptotic cell death by assisting in the degradation of important cellular proteins. |
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Authors:
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J K Newcomb-Fernandez; X Zhao; B R Pike; K K Wang; A Kampfl; R Beer; S M DeFord; R L Hayes |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism Volume: 21 ISSN: 0271-678X ISO Abbreviation: J. Cereb. Blood Flow Metab. Publication Date: 2001 Nov |
Date Detail:
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Created Date: 2001-11-09 Completed Date: 2001-12-18 Revised Date: 2007-11-15 |
Medline Journal Info:
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Nlm Unique ID: 8112566 Medline TA: J Cereb Blood Flow Metab Country: United States |
Other Details:
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Languages: eng Pagination: 1281-94 Citation Subset: IM |
Affiliation:
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Department of Neurosurgery, The Vivian L. Smith Center for Neurologic Research, University of Texas Health Science Center, Houston, Texas, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects, physiology Blotting, Western Calpain / antagonists & inhibitors, metabolism* Caspase 3 Caspases / antagonists & inhibitors, metabolism* Cells, Cultured Enzyme Activation / physiology Enzyme Inhibitors / pharmacology Fusobacterium Infections Glucose / pharmacology* Hippocampus / cytology Neuroglia / cytology, drug effects, enzymology Neurons / cytology, drug effects, enzymology* Oxygen / pharmacology* Phenotype Rats Reperfusion Injury / enzymology, pathology Rosette Formation Septum of Brain / cytology Spectrin / metabolism Stroke / enzymology, pathology |
| Grant Support | |
ID/Acronym/Agency:
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R01 NS39091/NS/NINDS NIH HHS; R01 NS40182/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Enzyme Inhibitors; 12634-43-4/Spectrin; 50-99-7/Glucose; 7782-44-7/Oxygen; EC 3.4.22.-/Calpain; EC 3.4.22.-/Casp3 protein, rat; EC 3.4.22.-/Caspase 3; EC 3.4.22.-/Caspases |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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