Source:http://linkedlifedata.com/resource/pubmed/id/17867433
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004112,
umls-concept:C0010453,
umls-concept:C0028128,
umls-concept:C0030685,
umls-concept:C0034693,
umls-concept:C0034721,
umls-concept:C0205263,
umls-concept:C0206116,
umls-concept:C0242184,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1456820,
umls-concept:C1963578
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pubmed:issue |
3
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pubmed:dateCreated |
2007-9-17
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pubmed:abstractText |
Hypoxia/reoxygenation (H/R) elicits neuronal cell injury and glial cell activation within the central nervous system (CNS). Neuroinflammation is a process that primarily results from the acute or chronic activation of glial cells. This overactive state of glial cells results in the increased release of nitric oxide (NO) and/or tumor necrosis factor alpha (TNF-alpha), a process which can lead to neuronal damage or death. In this study, we found that hypoxia for eight or twelve hours (h) followed by 24 h reoxygenation (H8/ R24 or H12/R24) induced NO production and TNF-alpha release from cultures of enriched microglial or mixed glial cells. However, microglial cells could not survive longer periods of hypoxia (> or = 12 h) in microglia-enriched culture. While astrocytes retained a 95% viability following longer periods of H/R in astrocyte-enriched cultures, they did not produce any significant quantities of NO and TNF-alpha. Reoxygenation for prolonged periods (three and five days) following H24 resulted in progressively greater increases in NO production (about two-fold greater level in hypoxia as compared to normoxic conditions) accompanied by relatively less increases in TNF-alpha release in mixed glial cell cultures. Our data indicate that inflammatory mediators such as NO and TNF-alpha are released from glia-enriched mix culture in response to H/R. While microglial cells are more vulnerable than astrocytes during H/R, they survive longer in the presence of astrocyte and are the major cell type producing NO and TNF-alpha. Furthermore, the TNF-alpha release precedes NO production in response to a prolonged duration of reoxygenation following hypoxia for 24 h.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jun
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pubmed:issn |
0304-4920
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
30
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pubmed:volume |
50
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
127-34
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pubmed:dateRevised |
2009-8-12
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pubmed:meshHeading |
pubmed-meshheading:17867433-Animals,
pubmed-meshheading:17867433-Astrocytes,
pubmed-meshheading:17867433-Cell Hypoxia,
pubmed-meshheading:17867433-Cell Survival,
pubmed-meshheading:17867433-Cells, Cultured,
pubmed-meshheading:17867433-Microglia,
pubmed-meshheading:17867433-Nitric Oxide,
pubmed-meshheading:17867433-Oxygen,
pubmed-meshheading:17867433-Rats,
pubmed-meshheading:17867433-Time Factors,
pubmed-meshheading:17867433-Tumor Necrosis Factor-alpha
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pubmed:year |
2007
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pubmed:articleTitle |
Hypoxia/Reoxygenation induces nitric oxide and TNF-alpha release from cultured microglia but not astrocytes of the rat.
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pubmed:affiliation |
Basic Medical Science, Department of Nursing Hung-Kuang University, Taichung, Taiwan, Republic of China.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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