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A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain

BACKGROUND: Neuropathic pain is a significant complication of nerve injury. This study aimed to conduct bioinformatics analysis of differentially expressed genes (DEGs) in microarrays of dorsal root ganglia (DRG) from rat models of neuropathic pain, based on 4 GEO datasets: GSE15041, GSE38038, GSE28...

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Autores principales: Wu, Yongle, Nie, Hai
Formato: Online Artículo Texto
Lenguaje:English
Publicado: International Scientific Literature, Inc. 2022
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8857866/
https://www.ncbi.nlm.nih.gov/pubmed/35165251
http://dx.doi.org/10.12659/MSM.934122
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author Wu, Yongle
Nie, Hai
author_facet Wu, Yongle
Nie, Hai
author_sort Wu, Yongle
collection PubMed
description BACKGROUND: Neuropathic pain is a significant complication of nerve injury. This study aimed to conduct bioinformatics analysis of differentially expressed genes (DEGs) in microarrays of dorsal root ganglia (DRG) from rat models of neuropathic pain, based on 4 GEO datasets: GSE15041, GSE38038, GSE2884, and GSE24982. MATERIAL/METHODS: We retrieved the 4 microarray datasets, which were generated using DRG samples collected in the early and late stages after spinal nerve ligation in rats. The common DEGs (co-DEGs) were identified and then subjected to Gene Ontology, pathway enrichment, and Protein–protein interaction network analyses. Drugs targeting the identified hub genes were analyzed using the Drug Gene Interaction Database. RESULTS: We identified 75 early-stage co-DEGs, which were enriched in chromosome segregation and protein catabolic processes, cytosol and extracellular exosome components, and ATP binding function and metabolic pathways. We identified 29 late-stage co-DEGs, which were enriched in protein tetramerization and drug responses, extracellular and membrane raft components, and protein homodimerization and binding functions and calcium signaling pathways. We also identified several hub genes, including Snap25 (synaptosome-associated protein of 25 kDa), Vamp2 (vesicle associated membrane protein 2), and Sf3b1 (splicing factor 3b subunit 1), the first 2 of which can be targeted by botulinum toxin derivatives. SNAP25 plays a role in synaptogenesis and the exocytotic release of neurotransmitters, and VAMP2 participates in neurotransmitter release at a step between docking and fusion. CONCLUSIONS: The present study reveals new mechanisms of neuropathic pain and provides key genes, including SNAP25 and VAMP2, for future studies.
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spelling pubmed-88578662022-03-09 A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain Wu, Yongle Nie, Hai Med Sci Monit Database Analysis BACKGROUND: Neuropathic pain is a significant complication of nerve injury. This study aimed to conduct bioinformatics analysis of differentially expressed genes (DEGs) in microarrays of dorsal root ganglia (DRG) from rat models of neuropathic pain, based on 4 GEO datasets: GSE15041, GSE38038, GSE2884, and GSE24982. MATERIAL/METHODS: We retrieved the 4 microarray datasets, which were generated using DRG samples collected in the early and late stages after spinal nerve ligation in rats. The common DEGs (co-DEGs) were identified and then subjected to Gene Ontology, pathway enrichment, and Protein–protein interaction network analyses. Drugs targeting the identified hub genes were analyzed using the Drug Gene Interaction Database. RESULTS: We identified 75 early-stage co-DEGs, which were enriched in chromosome segregation and protein catabolic processes, cytosol and extracellular exosome components, and ATP binding function and metabolic pathways. We identified 29 late-stage co-DEGs, which were enriched in protein tetramerization and drug responses, extracellular and membrane raft components, and protein homodimerization and binding functions and calcium signaling pathways. We also identified several hub genes, including Snap25 (synaptosome-associated protein of 25 kDa), Vamp2 (vesicle associated membrane protein 2), and Sf3b1 (splicing factor 3b subunit 1), the first 2 of which can be targeted by botulinum toxin derivatives. SNAP25 plays a role in synaptogenesis and the exocytotic release of neurotransmitters, and VAMP2 participates in neurotransmitter release at a step between docking and fusion. CONCLUSIONS: The present study reveals new mechanisms of neuropathic pain and provides key genes, including SNAP25 and VAMP2, for future studies. International Scientific Literature, Inc. 2022-02-15 /pmc/articles/PMC8857866/ /pubmed/35165251 http://dx.doi.org/10.12659/MSM.934122 Text en © Med Sci Monit, 2022 https://creativecommons.org/licenses/by-nc-nd/4.0/This work is licensed under Creative Common Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0 (https://creativecommons.org/licenses/by-nc-nd/4.0/) )
spellingShingle Database Analysis
Wu, Yongle
Nie, Hai
A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain
title A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain
title_full A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain
title_fullStr A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain
title_full_unstemmed A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain
title_short A Bioinformatics Study of Differentially Expressed Genes in Microarrays of Dorsal Root Ganglia from Rat Models of Neuropathic Pain
title_sort bioinformatics study of differentially expressed genes in microarrays of dorsal root ganglia from rat models of neuropathic pain
topic Database Analysis
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8857866/
https://www.ncbi.nlm.nih.gov/pubmed/35165251
http://dx.doi.org/10.12659/MSM.934122
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