Source:http://linkedlifedata.com/resource/pubmed/id/17330989
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Predicate | Object |
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rdf:type | |
lifeskim:mentions |
umls-concept:C0004112,
umls-concept:C0007018,
umls-concept:C0018969,
umls-concept:C0027882,
umls-concept:C0030685,
umls-concept:C0162638,
umls-concept:C0205263,
umls-concept:C0228174,
umls-concept:C0332307,
umls-concept:C0391871,
umls-concept:C0680255,
umls-concept:C1283071,
umls-concept:C1706276,
umls-concept:C1963578
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pubmed:issue |
5
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pubmed:dateCreated |
2007-4-30
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pubmed:abstractText |
To study a putative paracellular protective mechanism of astrocytes for neurons, immunohistochemical analysis was performed in ischemic rat brain, which colocalized with the expression of heme oxygase-1 (HO- 1) in astroglias surrounding dying TUNEL-positive neurons. As an in vitro paradigm for ischemia, cultured astrocytes were exposed to normobaric hypoxia (pO(2) asymptotically equal to 10 torr), which triggered marked increase in the expression of a 33 kDa stress protein, identified as HO-1. Induction of HO-1 message was observed within 4 h of hypoxia and peaked at 12 h, accompanied by an accelerated transcription of HO-1 message. Consistent with the induction of HO-1, a platelet bioassay revealed production of carbon monoxide by reoxygenated astrocytes. The presence of CO in the medium decelerated the hypoxia-mediated apoptotic type of cell death in cultured cerebral neurons via lowering the activity of caspase-3, a key enzyme regulating apoptotic cell death. This protection against apoptosis was likely mediated by CO-mediated increases in intracellular cGMP, because exposure of hypoxic neurons to CO increased intracellular cGMP levels, and addition of cGMP analogue to hypoxic neuronal cultures suppressed caspase-3 activity and promoted neuronal survival. These data describe a potentially important paracellular pathway through which astrocytes may rescue nearby neurons from ischemic death.
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pubmed:grant | |
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 |
May
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pubmed:issn |
1523-0864
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
9
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
543-52
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pubmed:dateRevised |
2007-12-3
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pubmed:meshHeading |
pubmed-meshheading:17330989-Animals,
pubmed-meshheading:17330989-Apoptosis,
pubmed-meshheading:17330989-Astrocytes,
pubmed-meshheading:17330989-Brain,
pubmed-meshheading:17330989-Brain Ischemia,
pubmed-meshheading:17330989-Carbon Monoxide,
pubmed-meshheading:17330989-Cell Hypoxia,
pubmed-meshheading:17330989-Cell Survival,
pubmed-meshheading:17330989-Cells, Cultured,
pubmed-meshheading:17330989-Heme Oxygenase-1,
pubmed-meshheading:17330989-Male,
pubmed-meshheading:17330989-Neurons,
pubmed-meshheading:17330989-Oxygen,
pubmed-meshheading:17330989-Rats,
pubmed-meshheading:17330989-Rats, Sprague-Dawley
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pubmed:year |
2007
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pubmed:articleTitle |
Hypoxia-mediated induction of heme oxygenase type I and carbon monoxide release from astrocytes protects nearby cerebral neurons from hypoxia-mediated apoptosis.
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pubmed:affiliation |
Department of Medicine, Seiwa Hospital, Osaka, Japan.
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural
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