Bioinformatics analysis of gene expression in Mesio-temporal lobe epilepsy_Journal of Epilepsy

Authors：

LI Yinchao ¹ , LIN Wanron ¹ , ZHAO Yiran ¹ , CHEN Shuda ¹ ,  ZHOU Liemin ^1,2

1. Department of Neurology, The Seven Affiliated Hospital, Sun Yat-Sen University, Shenzhen, Guangdong Province, 518107, China;
2. Department of Neurology, The First Affiliated Hospital, Sun Yat-Sen University, Guangzhou, Guangdong Province, 510030, China;

Corresponding author：

ZHOU Liemin, Email: lmzhou56@163.com

Keywords：

Bioinformatical analysis; Mesio-temporal lobe epilepsy; Hippocampus; Gene chip

DOI：

10.7507/2096-0247.20200032

Video：

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Objective To investigate the significant genes in Mesio-temporal lobe epilepsy (MTLE) and explore the molecular mechanism of MTLE.Methods The microarray data of MTLE were downloaded from the Gene Expression Omnibus (GEO) database and analyzed by bioinformatics methods using GEO2R tool, Venny2.1.0, FUNRICH and Cytoscape software, DAVID and String databases.Results Of all the 331 differentially expressed genes(DEGs), 46 genes were down-regulated and 285 genes were up-regulated in dataset GSE88992; Furthermore, the core module genes were identified from those DEGs, which were expressed mostly in plasma membrane and extracellular space; The major molecular funtion were chemokine activity, cytokine activity and chemokine receptor binding; The main biological pathways involved neutrophil chemotaxis, inflammatory response and positive regulation of ERK1 and ERK2 cascade; The KEGG analysis showed DEGs enriched in Chemokine signaling pathway, Cytokine-cytokine receptor interaction and Complement and coagulation cascades. In addition, ten hub genes (Il6, Fos, Stat3, Ptgs2, Ccl2, Timp1, Cd44, Icam1, Atf3, Cxcl1) were found to significantly express in the MTLE.Conclusion The pathogenesis of MTLE involves multiple genes, and multiple cell signaling pathways. Thus investigations of these genes may provide valuable insights into the mechanism of MTLE.

Citation： LI Yinchao, LIN Wanron, ZHAO Yiran, CHEN Shuda, ZHOU Liemin. Bioinformatics analysis of gene expression in Mesio-temporal lobe epilepsy. Journal of Epilepsy, 2020, 6(3): 181-187. doi: 10.7507/2096-0247.20200032 Copy

1.	Beghi E, Giussani G. Aging and the epidemiology of Epilepsy. Neuroepidemiology, 2018, 51(3-4): 216-223.
2.	Tang F, Hartz AMS, Bauer B. Drug-resistant epilepsy: multiple hypotheses, Ffew answers. Front Neurol, 2017, 8: 301.
3.	Kalozoumi G, Kel-Margoulis O, Vafiadaki E, et al. Glial responses during epileptogenesis in Mus musculus point to potential therapeutic targets. PLoS One, 2018, 13(8): e0201742.
4.	Pathan M, Keerthikumar S, Chisanga D, et al. A novel community driven software for functional enrichment analysis of extracellular vesicles data. J Extracell Vesicles, 2017, 6(1): 1321455.
5.	Szklarczyk D, Gable AL, Lyon D, et al. STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. Nucleic Acids Res, 2019, 47(D1): D607-D13.
6.	Shannon P, Markiel A, Ozier O, et al. Cytoscape: a software environment for integrated models of biomolecular interaction networks. Genome Res, 2003, 13(11): 2498-2504.
7.	Lauxmann S, Boutry-Kryza N, Rivier C, et al. An SCN2A mutation in a family with infantile seizures from Madagascar reveals an increased subthreshold Na(+) current. Epilepsia, 2013, 54(9): e117-121.
8.	Arlier Z, Bayri Y, Kolb LE, et al. Four novel SCN1A mutations in Turkish patients with severe myoclonic epilepsy of infancy (SMEI). Journal of Child Neurology, 2010, 25(10): 1265-1268.
9.	Rozycka A, Dorszewska J, Steinborn B, et al. Association study of the 2-bp deletion polymorphism in exon 6 of the CHRFAM7A gene with idiopathic generalized epilepsy. DNA Cell Biol, 2013, 32(11): 640-647.
10.	Michelucci R, Pulitano P, Di Bonaventura C, et al. The clinical phenotype of autosomal dominant lateral temporal lobe epilepsy related to reelin mutations. Epilepsy Behavior, 2017, 68: 103-107.
11.	Koh S. Role of neuroinflammation in evolution of childhood epilepsy. Journal of Child Neurology, 2018, 33(1): 64-72.
12.	Bien CG, Urbach H, Schramm J, et al. Limbic encephalitis as a precipitating event in adult-onset temporal lobe epilepsy. Neurology, 2007, 69(12): 1236-1244.
13.	Ricken G, Schwaiger C, De Simoni D, et al. Detection methods for autoantibodies in suspected autoimmune encephalitis. Front Neurol, 2018, 9: 841.
14.	Moscato EH, Peng X, Jain A, et al. Acute mechanisms underlying antibody effects in anti-N-methyl-D-aspartate receptor encephalitis. Ann Neurol, 2014, 76(1): 108-119.
15.	Vincent A, Bien CG, Irani SR, Waters P. Autoantibodies associated with diseases of the CNS: new developments and future challenges. Lancet Neurol, 2011, 10(8): 759-772.

1. Beghi E, Giussani G. Aging and the epidemiology of Epilepsy. Neuroepidemiology, 2018, 51(3-4): 216-223.
2. Tang F, Hartz AMS, Bauer B. Drug-resistant epilepsy: multiple hypotheses, Ffew answers. Front Neurol, 2017, 8: 301.
3. Kalozoumi G, Kel-Margoulis O, Vafiadaki E, et al. Glial responses during epileptogenesis in Mus musculus point to potential therapeutic targets. PLoS One, 2018, 13(8): e0201742.
4. Pathan M, Keerthikumar S, Chisanga D, et al. A novel community driven software for functional enrichment analysis of extracellular vesicles data. J Extracell Vesicles, 2017, 6(1): 1321455.
5. Szklarczyk D, Gable AL, Lyon D, et al. STRING v11: protein-protein association networks with increased coverage, supporting functional discovery in genome-wide experimental datasets. Nucleic Acids Res, 2019, 47(D1): D607-D13.
6. Shannon P, Markiel A, Ozier O, et al. Cytoscape: a software environment for integrated models of biomolecular interaction networks. Genome Res, 2003, 13(11): 2498-2504.
7. Lauxmann S, Boutry-Kryza N, Rivier C, et al. An SCN2A mutation in a family with infantile seizures from Madagascar reveals an increased subthreshold Na(+) current. Epilepsia, 2013, 54(9): e117-121.
8. Arlier Z, Bayri Y, Kolb LE, et al. Four novel SCN1A mutations in Turkish patients with severe myoclonic epilepsy of infancy (SMEI). Journal of Child Neurology, 2010, 25(10): 1265-1268.
9. Rozycka A, Dorszewska J, Steinborn B, et al. Association study of the 2-bp deletion polymorphism in exon 6 of the CHRFAM7A gene with idiopathic generalized epilepsy. DNA Cell Biol, 2013, 32(11): 640-647.
10. Michelucci R, Pulitano P, Di Bonaventura C, et al. The clinical phenotype of autosomal dominant lateral temporal lobe epilepsy related to reelin mutations. Epilepsy Behavior, 2017, 68: 103-107.
11. Koh S. Role of neuroinflammation in evolution of childhood epilepsy. Journal of Child Neurology, 2018, 33(1): 64-72.
12. Bien CG, Urbach H, Schramm J, et al. Limbic encephalitis as a precipitating event in adult-onset temporal lobe epilepsy. Neurology, 2007, 69(12): 1236-1244.
13. Ricken G, Schwaiger C, De Simoni D, et al. Detection methods for autoantibodies in suspected autoimmune encephalitis. Front Neurol, 2018, 9: 841.
14. Moscato EH, Peng X, Jain A, et al. Acute mechanisms underlying antibody effects in anti-N-methyl-D-aspartate receptor encephalitis. Ann Neurol, 2014, 76(1): 108-119.
15. Vincent A, Bien CG, Irani SR, Waters P. Autoantibodies associated with diseases of the CNS: new developments and future challenges. Lancet Neurol, 2011, 10(8): 759-772.

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