Gene Expression Profiling of the Sciatic Nerve in Streptozotocin-Induced Diabetic Rats with Peripheral Neuropathy
Aims. To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN). Methods. Diabetes in Sprague-Dawley rats was induced with streptozotocin (STZ) treatment, followed with neurological tests and histological examina...
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Published in | Journal of Diabetes Research Vol. 2020; no. 2020; pp. 1 - 14 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Cairo, Egypt
Hindawi Publishing Corporation
2020
Hindawi Hindawi Limited Wiley |
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Abstract | Aims. To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN). Methods. Diabetes in Sprague-Dawley rats was induced with streptozotocin (STZ) treatment, followed with neurological tests and histological examinations to assess the neuropathic symptoms of DPN. Microarray was performed on the sciatic nerve tissues from control rats and DPN rats at then6th week after diabetes induction, and differentially expressed genes (DEGs) between them were identified and applied for further bioinformatic analyses. Results. Experimental DPN rats were successfully constructed, presenting significantly decreased withdrawal threshold and motor nerve conduction velocity, and typical histological changes in the sciatic nerve. 597 DEGs (186 up- and 411 downregulated) were identified in DPN rats. DEGs from the 3 most highly connected clusters in the protein-protein interaction network were enriched for biological processes or pathways such as “cell division,” “cell cycle,” “protein phosphorylation,” “chemokine signaling pathway,” “neuropeptide signaling pathway,” “response to drug,” “cellular response to insulin stimulus,” “PPAR signaling pathway,” and “glycerophospholipid metabolism.” Thirteen genes were identified as the hub DEGs in the PPI network. Eleven transcriptional factors (TFs) targeting 9 of the 13 hub DEGs were predicted. Conclusions. The present study identified a pool of candidate biomarkers such as Cdk1, C3, Mapk12, Agt, Adipoq, Cxcl2, and Mmp9 and molecular mechanisms which may be involved in the early phase of experimental DPN. The findings provide clues for exploring new strategies for the early diagnosis and treatment of DPN. |
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AbstractList | Aims. To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN). Methods. Diabetes in Sprague-Dawley rats was induced with streptozotocin (STZ) treatment, followed with neurological tests and histological examinations to assess the neuropathic symptoms of DPN. Microarray was performed on the sciatic nerve tissues from control rats and DPN rats at then6th week after diabetes induction, and differentially expressed genes (DEGs) between them were identified and applied for further bioinformatic analyses. Results. Experimental DPN rats were successfully constructed, presenting significantly decreased withdrawal threshold and motor nerve conduction velocity, and typical histological changes in the sciatic nerve. 597 DEGs (186 up- and 411 downregulated) were identified in DPN rats. DEGs from the 3 most highly connected clusters in the protein-protein interaction network were enriched for biological processes or pathways such as “cell division,” “cell cycle,” “protein phosphorylation,” “chemokine signaling pathway,” “neuropeptide signaling pathway,” “response to drug,” “cellular response to insulin stimulus,” “PPAR signaling pathway,” and “glycerophospholipid metabolism.” Thirteen genes were identified as the hub DEGs in the PPI network. Eleven transcriptional factors (TFs) targeting 9 of the 13 hub DEGs were predicted. Conclusions. The present study identified a pool of candidate biomarkers such as Cdk1, C3, Mapk12, Agt, Adipoq, Cxcl2, and Mmp9 and molecular mechanisms which may be involved in the early phase of experimental DPN. The findings provide clues for exploring new strategies for the early diagnosis and treatment of DPN. Aims . To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN). Methods . Diabetes in Sprague-Dawley rats was induced with streptozotocin (STZ) treatment, followed with neurological tests and histological examinations to assess the neuropathic symptoms of DPN. Microarray was performed on the sciatic nerve tissues from control rats and DPN rats at then6th week after diabetes induction, and differentially expressed genes (DEGs) between them were identified and applied for further bioinformatic analyses. Results . Experimental DPN rats were successfully constructed, presenting significantly decreased withdrawal threshold and motor nerve conduction velocity, and typical histological changes in the sciatic nerve. 597 DEGs (186 up- and 411 downregulated) were identified in DPN rats. DEGs from the 3 most highly connected clusters in the protein-protein interaction network were enriched for biological processes or pathways such as “cell division,” “cell cycle,” “protein phosphorylation,” “chemokine signaling pathway,” “neuropeptide signaling pathway,” “response to drug,” “cellular response to insulin stimulus,” “PPAR signaling pathway,” and “glycerophospholipid metabolism.” Thirteen genes were identified as the hub DEGs in the PPI network. Eleven transcriptional factors (TFs) targeting 9 of the 13 hub DEGs were predicted. Conclusions . The present study identified a pool of candidate biomarkers such as Cdk1 , C3 , Mapk12 , Agt , Adipoq , Cxcl2 , and Mmp9 and molecular mechanisms which may be involved in the early phase of experimental DPN. The findings provide clues for exploring new strategies for the early diagnosis and treatment of DPN. To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN). Diabetes in Sprague-Dawley rats was induced with streptozotocin (STZ) treatment, followed with neurological tests and histological examinations to assess the neuropathic symptoms of DPN. Microarray was performed on the sciatic nerve tissues from control rats and DPN rats at then6th week after diabetes induction, and differentially expressed genes (DEGs) between them were identified and applied for further bioinformatic analyses. Experimental DPN rats were successfully constructed, presenting significantly decreased withdrawal threshold and motor nerve conduction velocity, and typical histological changes in the sciatic nerve. 597 DEGs (186 up- and 411 downregulated) were identified in DPN rats. DEGs from the 3 most highly connected clusters in the protein-protein interaction network were enriched for biological processes or pathways such as "cell division," "cell cycle," "protein phosphorylation," "chemokine signaling pathway," "neuropeptide signaling pathway," "response to drug," "cellular response to insulin stimulus," "PPAR signaling pathway," and "glycerophospholipid metabolism." Thirteen genes were identified as the hub DEGs in the PPI network. Eleven transcriptional factors (TFs) targeting 9 of the 13 hub DEGs were predicted. The present study identified a pool of candidate biomarkers such as , , , , , , and and molecular mechanisms which may be involved in the early phase of experimental DPN. The findings provide clues for exploring new strategies for the early diagnosis and treatment of DPN. |
Audience | Academic |
Author | Zhang, Junhui Tu, Yiji Di, Zhenglin Chen, Zenggan Zhang, Feng Cai, Li |
AuthorAffiliation | 4 Department of Ophthalmology, Ningbo Eye Hospital, Ningbo 315040, China 1 Department of Joint Surgery, Ningbo Sixth Hospital, Ningbo 315040, China 3 Joseph M. Still Burn and Reconstruction Center, Jackson, Mississippi 39201, USA 2 Department of Orthopedic Surgery, Zhongshan Hospital, Fudan University, Shanghai 200030, China |
AuthorAffiliation_xml | – name: 2 Department of Orthopedic Surgery, Zhongshan Hospital, Fudan University, Shanghai 200030, China – name: 1 Department of Joint Surgery, Ningbo Sixth Hospital, Ningbo 315040, China – name: 4 Department of Ophthalmology, Ningbo Eye Hospital, Ningbo 315040, China – name: 3 Joseph M. Still Burn and Reconstruction Center, Jackson, Mississippi 39201, USA |
Author_xml | – sequence: 1 fullname: Zhang, Junhui – sequence: 2 fullname: Di, Zhenglin – sequence: 3 fullname: Zhang, Feng – sequence: 4 fullname: Chen, Zenggan – sequence: 5 fullname: Tu, Yiji – sequence: 6 fullname: Cai, Li |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/32566679$$D View this record in MEDLINE/PubMed |
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Cites_doi | 10.2337/db10-1541 10.1155/2017/8103904 10.3892/br.2018.1135 10.1210/en.2008-0869 10.1016/j.nbd.2014.10.015 10.1016/j.clinthera.2018.04.001 10.1016/j.expneurol.2018.03.011 10.3390/ijms18061321 10.1159/000499597 10.1093/ckj/sfu059 10.1196/annals.1372.004 10.2337/db15-0835 10.1038/nrneurol.2011.137 10.1016/j.ejphar.2016.02.007 10.1016/j.diabres.2004.05.010 10.1016/j.jdiacomp.2015.06.008 10.1007/s11910-014-0473-5 10.1016/S0304-3959(00)00490-5 10.1136/bmj.g1799 10.3390/nu12010250 10.1002/j.1532-2149.2013.00356.x 10.1523/JNEUROSCI.1880-05.2006 10.3892/ijmm.2018.3509 10.1038/s41572-019-0092-1 10.1007/s12013-013-9609-5 10.1016/B978-0-444-53480-4.00006-0 10.2337/dc16-2042 10.1186/1744-8069-10-47 10.1016/j.coph.2004.03.009 10.2147/DMSO.S209118 10.1161/01.RES.0000033523.08033.16 10.1001/jama.2015.13611 10.1016/j.expneurol.2011.04.002 10.1093/brain/awr228 10.1113/EP088069 10.2337/db09-0047 10.1517/14728222.2014.960844 10.1007/s12035-013-8537-0 10.1186/1744-8069-6-28 10.1097/01.jnen.0000228199.89420.90 10.1038/oby.2006.276 10.1111/j.1365-2265.2007.03063.x 10.1055/s-0037-1621723 10.1002/jbt.22508 |
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Copyright | Copyright © 2020 Yiji Tu et al. COPYRIGHT 2020 Hindawi Limited Copyright © 2020 Yiji Tu et al. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. Copyright © 2020 Yiji Tu et al. 2020 |
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References | 22 44 (4) 2014; 348 23 24 25 26 27 28 29 30 31 10 32 11 33 12 34 13 35 14 36 15 37 16 38 17 39 18 19 1 2 3 5 6 7 8 9 40 41 20 42 21 43 |
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Snippet | Aims. To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN).... To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN). Diabetes in... Aims . To investigate the candidate biomarkers and molecular mechanisms involved in the early phase of experimental diabetic peripheral neuropathy (DPN).... |
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SubjectTerms | Animals Diabetes Diabetes Mellitus, Experimental - chemically induced Diabetes Mellitus, Experimental - genetics Diabetes Mellitus, Experimental - metabolism Diabetes Mellitus, Experimental - pathology Diabetes therapy Diabetic Neuropathies - genetics Diabetic Neuropathies - metabolism Diabetic Neuropathies - pathology Diabetic neuropathy Duloxetine Gene expression Gene Expression Profiling Genes Genetic aspects Glucose Laboratory animals Male Microarray Analysis Ontology Peripheral neuropathy Protein-protein interactions Proteins Rats Rats, Sprague-Dawley Rodents Sciatic Nerve - metabolism Sciatic Nerve - pathology Software Streptozocin Transcription (Genetics) Transmission electron microscopy Type 2 diabetes |
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Title | Gene Expression Profiling of the Sciatic Nerve in Streptozotocin-Induced Diabetic Rats with Peripheral Neuropathy |
URI | https://search.emarefa.net/detail/BIM-1183198 https://dx.doi.org/10.1155/2020/5283284 https://www.ncbi.nlm.nih.gov/pubmed/32566679 https://www.proquest.com/docview/2407983982/abstract/ https://pubmed.ncbi.nlm.nih.gov/PMC7256683 https://doaj.org/article/b41bdf449357432f9248954f7e3ef63f |
Volume | 2020 |
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