Document Detail


Expression of bystin in reactive astrocytes induced by ischemia/reperfusion and chemical hypoxia in vitro.
MedLine Citation:
PMID:  18929647     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
In this study, we investigated the effects of ischemia/reperfusion and chemical hypoxia on the morphology, cell viability and expression of bystin and glial fibrillary acidic protein (GFAP) in primary cultured astrocytes which were prepared by the subculture method. The astrocytes in Hank's medium without glucose and serum (oxygen-glucose deprivation, ischemic cells) were first exposed to 1% O2 and then to 21% O2 (normoxia), or treated with different concentrations of CoCl2 or NaN3 for different periods. Relevant observations and measurements were then conducted. The findings showed that treatment with 1% O2 for 0.5 or 3 h could induce a characteristic 'reactive' morphology and a significant increase in cell viability and total protein amount. The western blot analysis showed that treatment with 1% O2 for 0.5 or 3 h also induced a significant increase in the expression of bystin and that the response of bystin to mild ischemia was much more sensitive than that of GFAP. Similar results were also found in the cells treated with mild chemical hypoxia. The data demonstrated for the first time that mild ischemia and hypoxia could activate astrocytes and that bystin is a much more sensitive marker in activated astrocytes induced by ischemia and hypoxia as compared to GFAP. The significant up-regulation of bystin suggests that bystin may play an important role in the activation of astrocytes as well as in the neuroprotective role of hypoxic and ischemic preconditioning.
Authors:
Du Fang; Zhu Li; Qian Zhong-ming; Wu Xiao Mei; Yung Wing Ho; Xu Wei Yuan; Ke Ya
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2008-09-26
Journal Detail:
Title:  Biochimica et biophysica acta     Volume:  1782     ISSN:  0006-3002     ISO Abbreviation:  Biochim. Biophys. Acta     Publication Date:  2008 Nov 
Date Detail:
Created Date:  2008-11-10     Completed Date:  2009-04-15     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0217513     Medline TA:  Biochim Biophys Acta     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  658-63     Citation Subset:  IM    
Affiliation:
Department of Neurobiology and Neurochemistry, Institute for Nautical Medicine and Jiangsu Key Laboratory of Neurogeneration, Nantong University, Nantong 226001, PR China
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MeSH Terms
Descriptor/Qualifier:
Animals
Animals, Newborn
Anoxia* / chemically induced,  metabolism
Antimutagenic Agents / pharmacology
Astrocytes / cytology,  drug effects,  metabolism*
Brain Ischemia / metabolism*
Cell Adhesion Molecules / metabolism*
Cell Shape
Cell Survival
Cells, Cultured
Cobalt / pharmacology
Glial Fibrillary Acidic Protein / metabolism
Mice
Reperfusion*
Chemical
Reg. No./Substance:
0/Antimutagenic Agents; 0/Bysl protein, mouse; 0/Cell Adhesion Molecules; 0/Glial Fibrillary Acidic Protein; 7440-48-4/Cobalt; 7646-79-9/cobaltous chloride

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