Correlative genes in intractable temporal lobe epilepsy
- VernacularTitle:难治性颞叶癫(癎)的相关基因表达谱
- Author:
Xunyi WU
;
Zhen HONG
;
Xiang GAO
;
Guoxing ZHU
;
Chuanzhen Lü
- Publication Type:Journal Article
- Keywords:
Epilepsy,temporal lobe;
Gene expression profiling;
Oligonueleotide array sequence analysis;
Adaptor proteins,single transducing;
Membrane glycoproteins;
Potassium channels,inwardly rectifying
- From:
Chinese Journal of Neurology
2008;41(5):318-323
- CountryChina
- Language:Chinese
-
Abstract:
Objective To survey gene expression profiles in nonlesional refractory temporal lobe epilepsy(TLE)and to further verify the difference of gene expression.thus to evaluate the possible molecular pathogenesis of this kind of epilepsy that can help to supply a new way for the diagnosis and treatment.Methods The TLE samples and control cases were studied by means of cDNA microarray consisting of 1 8 000 genes.Reverse transcription polymerase chain reaction(RT-PCR)Was performed to measure the expression alterations of SH3GL2.BTNN2A2 and KCNJ4 mRNA in temporal cortex samples from patients who had undergone temporal lobectomy surgery for intractable epilepsy.Tissue from 10 subjects who did not have epilepsy served as controls.Results The known genes differently expressed in those TLE samples involved immunity correlation factor genes,signal conduction genes,ion channel transportation genes;mitochondria function genes and SO on were identified.Among which.the expression of SH3GL2 mRNA Was significantly increased in epileptic brain(1.022±0.547)compared with the controls(0.446±0.171,t=-3.181).In TLE group(0.481±0.196),the expression of BTN2A2 mRNA was also significantly higher than that of control subjects(0.243±0.111,t=3.351).Compared with control group(O.795±0.112),the expression of KCNJ4 mRNA Was significantly decreased in TLE patients(0.438±0.178).Conclusions cDNA microarray is an efficient and high.throughout method to survey gene expression profiles in intractable temporal lobe epilepsy.The variation of those gene expressions might be a potential etiological agent for TLE that may offer a novel target for anticonvulsant therapy.
