Linked Life Data

16034371

Source:http://linkedlifedata.com/resource/pubmed/id/16034371

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2006-1-25
pubmed:abstractText
After intracerebral hemorrhage (ICH), many changes of gene transcription occur that may be important because they will contribute to understanding mechanisms of injury and recovery. Therefore, gene expression was assessed using Affymetrix microarrays in the striatum and the overlying cortex at 24 h after intracranial infusions of blood into the striatum of adult rats. Intracerebral hemorrhage regulated 369 of 8,740 transcripts as compared with saline-injected controls, with 104 regulated genes shared by the striatum and cortex. There were 108 upregulated and 126 downregulated genes in striatum, and 170 upregulated and 69 downregulated genes in the cortex. Real-time reverse transcriptase-polymerase chain reaction (RT-PCR) confirmed upregulation of IL-1-beta, Lipcortin 1 (annexin) and metallothionein 1,2, and downregulation of potassium voltage-gated channel, shaker-related subfamily, beta member 2 (Kcnab2). Of the functional groups of genes modulated by ICH, many metabolism and signal-transduction-related genes decreased in striatum but increased in adjacent cortex. In contrast, most enzyme, cytokine, chemokine, and immune response genes were upregulated in both striatum and in the cortex after ICH, likely in response to foreign proteins from the blood. A number of these genes may contribute to brain edema and cellular apoptosis caused by ICH. In addition, downregulation of growth factor pathways and the phosphatidylinositol 3-kinase (PI3K)/Akt pathway could also contribute to perihematoma cell death/apoptosis. Intracerebral hemorrhage-related downregulation of GABA-related genes and potassium channels might contribute to perihematoma cellular excitability and increased risk of post-ICH seizures. These genomic responses to ICH potentially provide new therapeutic targets for treatment.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Feb
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
26
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
230-52
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:16034371-Animals, pubmed-meshheading:16034371-Annexin A1, pubmed-meshheading:16034371-Brain, pubmed-meshheading:16034371-Cerebral Hemorrhage, pubmed-meshheading:16034371-Cluster Analysis, pubmed-meshheading:16034371-Disease Models, Animal, pubmed-meshheading:16034371-Down-Regulation, pubmed-meshheading:16034371-Gene Expression Profiling, pubmed-meshheading:16034371-Genomics, pubmed-meshheading:16034371-Growth Substances, pubmed-meshheading:16034371-Interleukin-1, pubmed-meshheading:16034371-Male, pubmed-meshheading:16034371-Metallothionein, pubmed-meshheading:16034371-Oligonucleotide Array Sequence Analysis, pubmed-meshheading:16034371-Phosphatidylinositol 3-Kinases, pubmed-meshheading:16034371-Potassium Channels, Voltage-Gated, pubmed-meshheading:16034371-Rats, pubmed-meshheading:16034371-Rats, Sprague-Dawley, pubmed-meshheading:16034371-Reverse Transcriptase Polymerase Chain Reaction, pubmed-meshheading:16034371-Transcription, Genetic, pubmed-meshheading:16034371-Up-Regulation, pubmed-meshheading:16034371-gamma-Aminobutyric Acid
pubmed:year
2006
pubmed:articleTitle
Brain genomics of intracerebral hemorrhage.
pubmed:affiliation
MIND Institute and Department of Neurology, University of California at Davis, Sacramento, California 95817, USA. aiglu@ucdavis.edu
pubmed:publicationType
Journal Article, Comparative Study, Research Support, N.I.H., Extramural