Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038220 (status epilepticus)
 7,272 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Although different mechanisms have been proposed, it has been suggested that apolipoprotein J (ApoJ) and metallothionein II (MTII), expressed by astrocytes, are protective proteins. Alterations in their expression may contribute to the involvement of astrocytes in epileptogenesis. We studied the expression of MTII and ApoJ genes 7 days following status epilepticus induced in rats by intra-amygdala injection of kainate (KA). ApoJ mRNA levels were increased in both cortex (77%, p < 0.01) and hippocampus (64%, p < 0.02), whereas, in contrast to previous findings 3 days after KA injection, DNA fragmentation was not detected on agarose gel electrophoresis. These results show that ApoJ is induced along with early genes during massive apoptosis, and remains induced after the acute phase. MTII mRNA levels were altered only in hippocampus (62%, p < 0.05), whereas KA-treated rats had no seizure for 7 days. The sustained induction of MTII mRNA shows that zinc homeostasis is not returned to normal or alternatively that astrocytes maintain an altered phenotype in spite of normal zinc release. Polyadenylated RNA and beta-actin mRNA levels were in contrast unaltered in cortex or hippocampus at this time point. These specific variations in ApoJ and MTII mRNA expression during the latent period suggest that they are part of long term biochemical and/or phenotypic alterations in astrocytes, following a single episode of severe seizures.
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PMID:Alterations of metallothionein II and apolipoprotein J mRNA levels in kainate-treated rats. 959 52

Voltage-gated sodium channels (VGSC) are important determinants of neuronal excitability which are implicated in the pathogenesis of epilepsy. Ankyrin-G contributes to the distribution and regulation of VGSC. Here we investigated the alterations of the two alpha-subunits SCN8A and SCN1A and their adapter ankyrin-G in the hippocampal cornu ammonis 1 (CA1) of rats after pilocarpine induced status epilepticus (PISE), compared to the sham-control group (C1) and blank-control group (C2). Significant increase of SCN8A mRNA (41.08% increase compared to C1, P<0.001; 30.88% increase compared to C2, P=0.011) was detected 60 days after PISE. At D1 SCN8A mRNA reduced but no significant changes were detected when compared to controls (one-way ANOVA, F=1.232, P=0.276). After measuring the optical density of Western blot, we detected significant differences between the levels of SCN8A protein in different groups but no difference between the protein levels of SCN1A at D1 and D60 after pilocarpine treatment compared to the control. At D60 the relative copies of ankyrin-G mRNA on internal control beta-actin in PISE group increased significantly compared to C1 and C2 (one-way ANOVA, F=16.537, P<0.001). Significantly increase of ankyrin-G immunoreactivity in Western blot from the PISE group 1 day and 60 days after PISE was observed, compared to the controls (one-way ANOVA, F=24.255 at D1, P<0.001; F=29.280 at D60, P<0.001). After analyzing the double-stained cells counting, we detected significant differences between the numbers of SCN8A+/ankyrin-G+ immunoreactive cells in different groups in acute and chronic period following PISE (two way-ANOVA, F(group)=37.905, P<0.001; F(day)=45.310, P<0.001). The data revealed that both SCN8A and ankyrin-G increased significantly in the CA1 subfield of the rat hippocampus 60 days following pilocarpine induced status epilepticus and co-localized with each other.
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PMID:Long-term increasing co-localization of SCN8A and ankyrin-G in rat hippocampal cornu ammonis 1 after pilocarpine induced status epilepticus. 1930 53

Reference genes are often used to normalize expression of data from real-time quantitative reverse transcription-polymerase chain reaction (RT-qPCR), and only a validation of their stability during a given experimental paradigm leads to reliable interpretations. The present study was thus designed to validate potential reference genes in a mouse model of mesiotemporal lobe epilepsy (MTLE) with focal seizures after unilateral intrahippocampal injection of kainate (KA). Ipsilateral and contralateral hippocampi were removed during nonconvulsive status epilepticus (5 hr), epileptogenesis (7 days), and the chronic period of recurrent focal seizures (21 days). Naive animals were equally studied. The stability of eight potential reference genes (hypoxanthine phosphoribosyltransferase, Hprt1; peptidylprolyl isomerase A, Ppia; TATA box binding protein, Tbp; beta-actin, Actb; acidic ribosomal phosphoprotein P0, Arbp; glyceraldehyde-3-phosphate dehydrogenase, Gapdh; ribosomal RNA 18S, 18S rRNA; and glucuronidase beta, Gusb) were determined using geNorm and NormFinder software. The first five (Hprt1, Ppia, Tbp, Actb, and Arbp) were found to be stable across the different phases of the disease and appeared adequate for normalizing RT-qPCR data in this model. This was in contrast to the other three (18S rRNA, Gapdh, and Gusb), which showed unstable expressions and should be avoided. The analysis of KA-induced changes in the expression of glial fibrillary acidic protein (Gfap) gene resulted in various relative expressions or even a completely different pattern when unstable reference genes were used. These results highlight the absolute need to validate the reference genes for a correct interpretation of mRNA quantification.
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PMID:Selection of reference genes for real-time quantitative reverse transcription-polymerase chain reaction in hippocampal structure in a murine model of temporal lobe epilepsy with focal seizures. 1993 10