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Identification of novel gene and pathway targets for human epilepsy treatment

BACKGROUND: The aim of this study was to explore epilepsy-related mechanism so as to figure out the possible targets for epilepsy treatment. METHODS: The gene expression profile dataset GES32534 was downloaded from Gene Expression Omnibus database. We identified the differentially expressed genes (D...

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Autores principales: Jin, Ying, Zhao, Chunzhe, Chen, Lihui, Liu, Xiangyu, Pan, Shuxiao, Ju, Dongsheng, Ma, Jing, Li, Jinying, Wei, Bo
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2016
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705636/
https://www.ncbi.nlm.nih.gov/pubmed/26742644
http://dx.doi.org/10.1186/s40659-015-0060-5
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author Jin, Ying
Zhao, Chunzhe
Chen, Lihui
Liu, Xiangyu
Pan, Shuxiao
Ju, Dongsheng
Ma, Jing
Li, Jinying
Wei, Bo
author_facet Jin, Ying
Zhao, Chunzhe
Chen, Lihui
Liu, Xiangyu
Pan, Shuxiao
Ju, Dongsheng
Ma, Jing
Li, Jinying
Wei, Bo
author_sort Jin, Ying
collection PubMed
description BACKGROUND: The aim of this study was to explore epilepsy-related mechanism so as to figure out the possible targets for epilepsy treatment. METHODS: The gene expression profile dataset GES32534 was downloaded from Gene Expression Omnibus database. We identified the differentially expressed genes (DEGs) by Affy package. Then the DEGs were used to perform gene ontology (GO) and pathway enrichment analyses. Furthermore, a protein–protein interaction (PPI) network was constructed with the DEGs followed by co-expression modules construction and analysis. RESULTS: Total 420 DEGs were screened out, including 214 up-regulated and 206 down-regulated genes. Functional enrichment analysis revealed that down-regulated genes were mainly involved in the process of immunity regulation and biological repairing process while up-regulated genes were closely related to transporter activity. PPI network analysis showed the top ten genes with high degrees were all down-regulated, among which FN1 had the highest degree. The up-regulated and down-regulated DEGs in the PPI network generated two obvious sub-co-expression modules, respectively. In up-co-expression module, SCN3B (sodium channel, voltage gated, type III beta subunit) was enriched in GO:0006814 ~ sodium ion transport. In down-co-expression module, C1QB (complement C1s), C1S (complement component 1, S subcomponent) and CFI (complement factor I) were enriched in GO:0006955 ~ immune response. CONCLUSION: The immune response and complement system play a major role in the pathogenesis of epilepsy. Additionally, C1QB, C1S, CFI, SCN3B and FN1 may be potential therapeutic targets for epilepsy.
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spelling pubmed-47056362016-01-09 Identification of novel gene and pathway targets for human epilepsy treatment Jin, Ying Zhao, Chunzhe Chen, Lihui Liu, Xiangyu Pan, Shuxiao Ju, Dongsheng Ma, Jing Li, Jinying Wei, Bo Biol Res Research Article BACKGROUND: The aim of this study was to explore epilepsy-related mechanism so as to figure out the possible targets for epilepsy treatment. METHODS: The gene expression profile dataset GES32534 was downloaded from Gene Expression Omnibus database. We identified the differentially expressed genes (DEGs) by Affy package. Then the DEGs were used to perform gene ontology (GO) and pathway enrichment analyses. Furthermore, a protein–protein interaction (PPI) network was constructed with the DEGs followed by co-expression modules construction and analysis. RESULTS: Total 420 DEGs were screened out, including 214 up-regulated and 206 down-regulated genes. Functional enrichment analysis revealed that down-regulated genes were mainly involved in the process of immunity regulation and biological repairing process while up-regulated genes were closely related to transporter activity. PPI network analysis showed the top ten genes with high degrees were all down-regulated, among which FN1 had the highest degree. The up-regulated and down-regulated DEGs in the PPI network generated two obvious sub-co-expression modules, respectively. In up-co-expression module, SCN3B (sodium channel, voltage gated, type III beta subunit) was enriched in GO:0006814 ~ sodium ion transport. In down-co-expression module, C1QB (complement C1s), C1S (complement component 1, S subcomponent) and CFI (complement factor I) were enriched in GO:0006955 ~ immune response. CONCLUSION: The immune response and complement system play a major role in the pathogenesis of epilepsy. Additionally, C1QB, C1S, CFI, SCN3B and FN1 may be potential therapeutic targets for epilepsy. BioMed Central 2016-01-07 /pmc/articles/PMC4705636/ /pubmed/26742644 http://dx.doi.org/10.1186/s40659-015-0060-5 Text en © Jin et al. 2016 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Research Article
Jin, Ying
Zhao, Chunzhe
Chen, Lihui
Liu, Xiangyu
Pan, Shuxiao
Ju, Dongsheng
Ma, Jing
Li, Jinying
Wei, Bo
Identification of novel gene and pathway targets for human epilepsy treatment
title Identification of novel gene and pathway targets for human epilepsy treatment
title_full Identification of novel gene and pathway targets for human epilepsy treatment
title_fullStr Identification of novel gene and pathway targets for human epilepsy treatment
title_full_unstemmed Identification of novel gene and pathway targets for human epilepsy treatment
title_short Identification of novel gene and pathway targets for human epilepsy treatment
title_sort identification of novel gene and pathway targets for human epilepsy treatment
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4705636/
https://www.ncbi.nlm.nih.gov/pubmed/26742644
http://dx.doi.org/10.1186/s40659-015-0060-5
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