Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:2.7.7.49 (reverse transcriptase)
 31,746 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The purpose of the present study is to examine spatial and temporal expression of P-glycoprotein in the brain of congenitally hydrocephalic HTX rats. P-glycoprotein has been reported not only as a drug efflux pump but also one of the factors that restricts brain edema. We examined the rat brain from postnatal day 1 to 60 using light and electron microscopy, immunohistochemistry, Western immunoblot and reverse transcriptase-polymerase chain reaction (RT-PCR) methods with monoclonal antibody specific for P-glycoprotein. Immunohistochemically, the positive anti-P-glycoprotein reactivity was found in capillaries of the normal control rat cerebrum. In the hydrocephalic HTX rat brains, it was also found in the capillaries, but only very weak to no reactivity was found in the capillaries of the spongy changes and cystic wall in the subcortical and lateral periventricular white matter. Immunoelectron microscopically, the reaction product was found exclusively on the luminal surface of the capillary endothelium in control rats. A tracer study with intracardiac perfusion of lanthanum chloride showed that lanthanum penetrated the tight junctions and passed through the intercellular space. In the Western immunoblot analysis, P-glycoprotein of 170 kDa was detected clearly in most normal control rat brains but it was not found in the hydrocephalic HTX rat brains. Moreover, mdr1 P-glycoprotein gene expression in the subcortical white matter was examined by RT-PCR. It was detected in all normal control rat brains, but not found in the hydrocephalic HTX rat brains. The results suggested that the absence of P-glycoprotein expression in the capillaries of deep subcortical and lateral periventricular white matter of hydrocephalic HTX rats led to a deficiency of the blood-brain barrier and might be related to vasogenic edema and to the formation of the spongy changes and cystic cavities.
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PMID:Spatial and temporal expression of P-glycoprotein in the congenitally hydrocephalic HTX rat brain. 883 57

It has been suggested that reduced astrocytic uptake of neuronally released glutamate contributes to the pathogenesis of hepatic encephalopathy in acute liver failure. In order to further address this issue, the recently cloned and sequenced astrocytic glutamate transporter GLT-1 was studied in brain preparations from rats with ischemic liver failure induced by portacaval anastomosis followed 24 h later by hepatic artery ligation and from appropriate sham-operated controls. GLT-1 expression was studied using reverse transcriptase-polymerase chain reaction (RT-PCR). Expression of GLT-1 transcript was significantly decreased in frontal cortex at coma stages of acute liver failure. Western blotting using a polyclonal antibody to GLT-1 revealed a concomitant decrease in expression of transporter protein in the brains of rats with acute liver failure. Reduced capacity of astrocytes to reuptake neuronally released glutamate, resulting from a GLT-1 transporter deficit and the consequently compromised neuron-astrocytic trafficking of glutamate could contribute to the pathogenesis of hepatic encephalopathy and brain edema, two major complications of acute liver failure.
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PMID:Decreased glutamate transporter (GLT-1) expression in frontal cortex of rats with acute liver failure. 923 93

The aim in this study was to investigate whether our experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could ameliorate disruption of microvascular integrity by reducing matrix metalloproteinase (MMP) expression during reperfusion. Stroke in Sprague Dawley rats (n = 42) was induced by a 2-h right middle cerebral artery (MCA) occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 24 of the ischemic rats received 6ml isotonic saline at 37 degrees C infused into the ischemic area through the filament. Brain edema was determined by comparing the percentage difference in brain volume between the right and left (contralateral to stroke site) hemispheres, while the expressions of MMP-2 and -9 mRNA were analyzed by real-time reverse transcriptase-polymerase chain reaction (real-time RT-PCR). A significant (p < 0.01) brain edema, determined by an increased brain volume of 19 +/- 4%, and overexpression of the mRNA encoding MMPs, determined by increased relative mRNA level ratio, were found in ischemic rats. The brain damage, in terms of brain edema (4 +/- 1%) and overexpression of MMPs, was significantly (p < 0.05) ameliorated as a result of saline flushing into the ischemic territory prior to reperfusion. This study has enhanced our understanding of the causal mechanisms by which the neuroprotective effect of ischemic area "flushing" can be achieved.
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PMID:Reduced brain edema and matrix metalloproteinase (MMP) expression by pre-reperfusion infusion into ischemic territory in rat. 1553 Oct 84

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.
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PMID:Brain genomics of intracerebral hemorrhage. 1603 71