Linked Life Data

17406657

Source:http://linkedlifedata.com/resource/pubmed/id/17406657

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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2007-9-20
pubmed:abstractText
Pronounced hyperglycemia provoked by extradural compression (EC) of the sensorimotor cortex was recently described in the non-insulin dependent Goto-Kakizaki (GK) diabetic rat. Compared with control Wistar rats, GK rats exhibited more extensive brain damage after cortical ischemia at 48 h of reperfusion (Moreira et al, 2007). We hypothesized that the enhanced brain injury in GK rats could be caused by differential regulation of the heme degrading enzyme heme oxygenase (HO)-1, known to interact with the expression of other target genes implicated in antioxidant defense, inflammation and neurodegeneration, such as superoxide dismutase (SOD)-1, -2, inducible nitric oxide synthase (iNOS), and tumor necrosis factor-alpha (TNFalpha). At 48 h after ischemia, relative mRNA expression of such target genes was compared between ipsilateral (compressed) and contralateral (uncompressed) hemispheres of GK rats, along with baseline comparison of sham, uncompressed GK and Wistar rats. Immunohistochemistry was performed to detect cellular and regional localization of HO-1 at this time point. Baseline expression of HO-1, iNOS, and TNFalpha mRNA was increased in the cortex of sham GK rats. GK rats showed pronounced hyperglycemia during EC and transient attenuation of regional cerebral blood flow recovery. At 48 h after reperfusion, HO-1 mRNA expression was 7- to 8-fold higher in the ischemic cortex of both strains, being the most upregulated gene under study. Heme oxygenase-1 protein expression was significantly reduced in diabetic rats and was found in perilesional astrocytes and rare microglial cells, in both strains. The reduced HO-1 protein expression in GK rats at 48 h after reperfusion combined with more extensive neurodegeneration induced by EC, provides further in vivo evidence for a neuroprotective role of HO after brain ischemia.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
27
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1710-23
pubmed:dateRevised
2009-11-3
pubmed:meshHeading
pubmed:year
2007
pubmed:articleTitle
Reduced HO-1 protein expression is associated with more severe neurodegeneration after transient ischemia induced by cortical compression in diabetic Goto-Kakizaki rats.
pubmed:affiliation
Division of Drug Dependence Research, Department of Clinical Neuroscience, Karolinska Institutet, Stockholm, Sweden.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't