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Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy

The present study aimed to explore novel target genes that regulate the development of diabetic neuropathy (DN) by analyzing gene expression profiles in the sciatic nerve of infected mice. The GSE11343 microarray dataset, which was downloaded from Gene Expression Omnibus, included data on 4 control...

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Autores principales: ZHANG, LEI, QU, SHEN, LIANG, AIBIN, JIANG, HONG, WANG, HAO
Formato: Online Artículo Texto
Lenguaje:English
Publicado: D.A. Spandidos 2015
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4292761/
https://www.ncbi.nlm.nih.gov/pubmed/25435094
http://dx.doi.org/10.3892/ijmm.2014.2011
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author ZHANG, LEI
QU, SHEN
LIANG, AIBIN
JIANG, HONG
WANG, HAO
author_facet ZHANG, LEI
QU, SHEN
LIANG, AIBIN
JIANG, HONG
WANG, HAO
author_sort ZHANG, LEI
collection PubMed
description The present study aimed to explore novel target genes that regulate the development of diabetic neuropathy (DN) by analyzing gene expression profiles in the sciatic nerve of infected mice. The GSE11343 microarray dataset, which was downloaded from Gene Expression Omnibus, included data on 4 control samples and 5 samples from mice with diabetes induced by streptozotocin (STZ), 5 samples from normal mice treated with rosiglitazone (Rosi) and 5 samples from mice with diabetes induced by STZ and treated with Rosi. Differentially expressed genes (DEGs) between the different groups were identified using the substitution augmentation modification redefinition (SAMR) model. The Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID). Regulatory and protein-protein interaction networks were searched using BioCarta and STRING, respectively. The protein structures of potential regulatory genes were predicted using the SYBYL program. Compared with the controls, 1,384 DEGs were identified in the mice with STZ-induced diabetes and 7 DEGs were identified in the mice treated with Rosi. There were 518 DEGs identified between the mice in the STZ + Rosi and STZ groups. We identified 45 GO items, and the calmodulin nerve phosphatase and chemokine signaling pathways were identified as the main pathways. Three genes [myristoylated alanine-rich protein kinase C substrate (Marcks), GLI pathogenesis-related 2 (Glipr2) and centrosomal protein 170 kDa (Cep170)] were found to be co-regulated by both STZ and Rosi, the protein structure of which was predicted and certain binding activity to Rosi was docked. Our study demonstrates that the Marcks, Glipr2 and Cep170 genes may be underlying drug targets in the treatment of DN.
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spelling pubmed-42927612016-02-01 Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy ZHANG, LEI QU, SHEN LIANG, AIBIN JIANG, HONG WANG, HAO Int J Mol Med Articles The present study aimed to explore novel target genes that regulate the development of diabetic neuropathy (DN) by analyzing gene expression profiles in the sciatic nerve of infected mice. The GSE11343 microarray dataset, which was downloaded from Gene Expression Omnibus, included data on 4 control samples and 5 samples from mice with diabetes induced by streptozotocin (STZ), 5 samples from normal mice treated with rosiglitazone (Rosi) and 5 samples from mice with diabetes induced by STZ and treated with Rosi. Differentially expressed genes (DEGs) between the different groups were identified using the substitution augmentation modification redefinition (SAMR) model. The Gene Ontology (GO) term and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses were performed using the Database for Annotation, Visualization and Integrated Discovery (DAVID). Regulatory and protein-protein interaction networks were searched using BioCarta and STRING, respectively. The protein structures of potential regulatory genes were predicted using the SYBYL program. Compared with the controls, 1,384 DEGs were identified in the mice with STZ-induced diabetes and 7 DEGs were identified in the mice treated with Rosi. There were 518 DEGs identified between the mice in the STZ + Rosi and STZ groups. We identified 45 GO items, and the calmodulin nerve phosphatase and chemokine signaling pathways were identified as the main pathways. Three genes [myristoylated alanine-rich protein kinase C substrate (Marcks), GLI pathogenesis-related 2 (Glipr2) and centrosomal protein 170 kDa (Cep170)] were found to be co-regulated by both STZ and Rosi, the protein structure of which was predicted and certain binding activity to Rosi was docked. Our study demonstrates that the Marcks, Glipr2 and Cep170 genes may be underlying drug targets in the treatment of DN. D.A. Spandidos 2015-02 2014-11-26 /pmc/articles/PMC4292761/ /pubmed/25435094 http://dx.doi.org/10.3892/ijmm.2014.2011 Text en Copyright © 2015, Spandidos Publications http://creativecommons.org/licenses/by/3.0 This is an open-access article licensed under a Creative Commons Attribution-NonCommercial 3.0 Unported License. The article may be redistributed, reproduced, and reused for non-commercial purposes, provided the original source is properly cited.
spellingShingle Articles
ZHANG, LEI
QU, SHEN
LIANG, AIBIN
JIANG, HONG
WANG, HAO
Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
title Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
title_full Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
title_fullStr Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
title_full_unstemmed Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
title_short Gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
title_sort gene expression microarray analysis of the sciatic nerve of mice with diabetic neuropathy
topic Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4292761/
https://www.ncbi.nlm.nih.gov/pubmed/25435094
http://dx.doi.org/10.3892/ijmm.2014.2011
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