Bioinformatics analysis of differentially expressed gene profiles associated with systemic lupus erythematosus
DNA microarray and high-throughput sequencing have been widely used to identify the differentially expressed genes (DEGs) in systemic lupus erythematosus (SLE). However, the big data from gene microarrays are also challenging to work with in terms of analysis and processing. The presents study combi...
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description | DNA microarray and high-throughput sequencing have been widely used to identify the differentially expressed genes (DEGs) in systemic lupus erythematosus (SLE). However, the big data from gene microarrays are also challenging to work with in terms of analysis and processing. The presents study combined data from the microarray expression profile (GSE65391) and bioinformatics analysis to identify the key genes and cellular pathways in SLE. Gene ontology (GO) and cellular pathway enrichment analyses of DEGs were performed to investigate significantly enriched pathways. A protein‑protein interaction network was constructed to determine the key genes in the occurrence and development of SLE. A total of 310 DEGs were identified in SLE, including 193 upregulated genes and 117 downregulated genes. GO analysis revealed that the most significant biological process of DEGs was immune system process. Kyoto Encyclopedia of Genes and Genome pathway analysis showed that these DEGs were enriched in signaling pathways associated with the immune system, including the RIG‑I‑like receptor signaling pathway, intestinal immune network for IgA production, antigen processing and presentation and the toll‑like receptor signaling pathway. The current study screened the top 10 genes with higher degrees as hub genes, which included 2'‑5'‑oligoadenylate synthetase 1, MX dynamin like GTPase 2, interferon induced protein with tetratricopeptide repeats 1, interferon regulatory factor 7, interferon induced with helicase C domain 1, signal transducer and activator of transcription 1, ISG15 ubiquitin‑like modifier, DExD/H‑box helicase 58, interferon induced protein with tetratricopeptide repeats 3 and 2'‑5'‑oligoadenylate synthetase 2. Module analysis revealed that these hub genes were also involved in the RIG‑I‑like receptor signaling, cytosolic DNA‑sensing, toll‑like receptor signaling and ribosome biogenesis pathways. In addition, these hub genes, from different probe sets, exhibited significant co‑expressed tendency in multi‑experiment microarray datasets (P |
doi_str_mv | 10.3892/mmr.2017.8293 |
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However, the big data from gene microarrays are also challenging to work with in terms of analysis and processing. The presents study combined data from the microarray expression profile (GSE65391) and bioinformatics analysis to identify the key genes and cellular pathways in SLE. Gene ontology (GO) and cellular pathway enrichment analyses of DEGs were performed to investigate significantly enriched pathways. A protein‑protein interaction network was constructed to determine the key genes in the occurrence and development of SLE. A total of 310 DEGs were identified in SLE, including 193 upregulated genes and 117 downregulated genes. GO analysis revealed that the most significant biological process of DEGs was immune system process. Kyoto Encyclopedia of Genes and Genome pathway analysis showed that these DEGs were enriched in signaling pathways associated with the immune system, including the RIG‑I‑like receptor signaling pathway, intestinal immune network for IgA production, antigen processing and presentation and the toll‑like receptor signaling pathway. The current study screened the top 10 genes with higher degrees as hub genes, which included 2'‑5'‑oligoadenylate synthetase 1, MX dynamin like GTPase 2, interferon induced protein with tetratricopeptide repeats 1, interferon regulatory factor 7, interferon induced with helicase C domain 1, signal transducer and activator of transcription 1, ISG15 ubiquitin‑like modifier, DExD/H‑box helicase 58, interferon induced protein with tetratricopeptide repeats 3 and 2'‑5'‑oligoadenylate synthetase 2. Module analysis revealed that these hub genes were also involved in the RIG‑I‑like receptor signaling, cytosolic DNA‑sensing, toll‑like receptor signaling and ribosome biogenesis pathways. In addition, these hub genes, from different probe sets, exhibited significant co‑expressed tendency in multi‑experiment microarray datasets (P<0.01). In conclusion, these key genes and cellular pathways may improve the current understanding of the underlying mechanism of development of SLE. These key genes may be potential biomarkers of diagnosis, therapy and prognosis for SLE.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2017.8293</identifier><identifier>PMID: 29257335</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Antigen presentation ; Antigen processing ; Bioinformatics ; Care and treatment ; Computational biology ; Datasets ; Development and progression ; Disease ; DNA helicase ; DNA microarrays ; DNA sequencing ; Dynamin ; Gene expression ; Genetic aspects ; Genomes ; Genotypes ; Guanosine triphosphatases ; Health aspects ; Immune system ; Immunoglobulin A ; Innovations ; Interferon regulatory factor ; Interferon regulatory factor 7 ; Intestine ; Lupus ; Next-generation sequencing ; Protein interaction ; Proteins ; Signal transduction ; Studies ; Systemic lupus erythematosus ; Toll-like receptors ; Transcription ; Ubiquitin</subject><ispartof>Molecular medicine reports, 2018-03, Vol.17 (3), p.3591-3598</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Wu et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-9a6adbfca483a990c106a8901521ed3d3f29528d33e8b1765f7e8e137dcdb1533</citedby><cites>FETCH-LOGICAL-c482t-9a6adbfca483a990c106a8901521ed3d3f29528d33e8b1765f7e8e137dcdb1533</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,315,782,786,887,27931,27932</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29257335$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wu, Chengjiang</creatorcontrib><creatorcontrib>Zhao, Yangjing</creatorcontrib><creatorcontrib>Lin, Yu</creatorcontrib><creatorcontrib>Yang, Xinxin</creatorcontrib><creatorcontrib>Yan, Meina</creatorcontrib><creatorcontrib>Min, Yujiao</creatorcontrib><creatorcontrib>Pan, Zihui</creatorcontrib><creatorcontrib>Xia, Sheng</creatorcontrib><creatorcontrib>Shao, Qixiang</creatorcontrib><title>Bioinformatics analysis of differentially expressed gene profiles associated with systemic lupus erythematosus</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>DNA microarray and high-throughput sequencing have been widely used to identify the differentially expressed genes (DEGs) in systemic lupus erythematosus (SLE). However, the big data from gene microarrays are also challenging to work with in terms of analysis and processing. The presents study combined data from the microarray expression profile (GSE65391) and bioinformatics analysis to identify the key genes and cellular pathways in SLE. Gene ontology (GO) and cellular pathway enrichment analyses of DEGs were performed to investigate significantly enriched pathways. A protein‑protein interaction network was constructed to determine the key genes in the occurrence and development of SLE. A total of 310 DEGs were identified in SLE, including 193 upregulated genes and 117 downregulated genes. GO analysis revealed that the most significant biological process of DEGs was immune system process. Kyoto Encyclopedia of Genes and Genome pathway analysis showed that these DEGs were enriched in signaling pathways associated with the immune system, including the RIG‑I‑like receptor signaling pathway, intestinal immune network for IgA production, antigen processing and presentation and the toll‑like receptor signaling pathway. The current study screened the top 10 genes with higher degrees as hub genes, which included 2'‑5'‑oligoadenylate synthetase 1, MX dynamin like GTPase 2, interferon induced protein with tetratricopeptide repeats 1, interferon regulatory factor 7, interferon induced with helicase C domain 1, signal transducer and activator of transcription 1, ISG15 ubiquitin‑like modifier, DExD/H‑box helicase 58, interferon induced protein with tetratricopeptide repeats 3 and 2'‑5'‑oligoadenylate synthetase 2. Module analysis revealed that these hub genes were also involved in the RIG‑I‑like receptor signaling, cytosolic DNA‑sensing, toll‑like receptor signaling and ribosome biogenesis pathways. In addition, these hub genes, from different probe sets, exhibited significant co‑expressed tendency in multi‑experiment microarray datasets (P<0.01). In conclusion, these key genes and cellular pathways may improve the current understanding of the underlying mechanism of development of SLE. These key genes may be potential biomarkers of diagnosis, therapy and prognosis for SLE.</description><subject>Antigen presentation</subject><subject>Antigen processing</subject><subject>Bioinformatics</subject><subject>Care and treatment</subject><subject>Computational biology</subject><subject>Datasets</subject><subject>Development and progression</subject><subject>Disease</subject><subject>DNA helicase</subject><subject>DNA microarrays</subject><subject>DNA sequencing</subject><subject>Dynamin</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Genomes</subject><subject>Genotypes</subject><subject>Guanosine triphosphatases</subject><subject>Health aspects</subject><subject>Immune system</subject><subject>Immunoglobulin A</subject><subject>Innovations</subject><subject>Interferon regulatory factor</subject><subject>Interferon regulatory factor 7</subject><subject>Intestine</subject><subject>Lupus</subject><subject>Next-generation sequencing</subject><subject>Protein interaction</subject><subject>Proteins</subject><subject>Signal transduction</subject><subject>Studies</subject><subject>Systemic lupus erythematosus</subject><subject>Toll-like receptors</subject><subject>Transcription</subject><subject>Ubiquitin</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptks2L1TAUxYsozji6dCsFN276zEfTJBthHPyCATe6DnnJzXsZ2qbmtmr_e1PmOToiWSRwf_eEczhV9ZySHVeavR6GvGOEyp1imj-ozqnUtOGEtA9Pb6a1PKueIN4Q0gkm9OPqjGkmJOfivBrfxhTHkPJg5-iwtqPtV4xYp1D7GAJkGOdo-36t4eeUARF8fYAR6imnEHsoK4jJRTuXwY84H2tccYYhurpfpgVryOt8hCKfcMGn1aNge4Rnp_ui-vr-3Zerj8315w-fri6vG9cqNjfadtbvg7Ot4lZr4ijprNKECkbBc88D04IpzzmoPZWdCBIUUC6983sqOL-o3tzqTst-AO-KiWx7M-U42LyaZKO5Pxnj0RzSdyMUYbRri8Crk0BO3xbA2QwRHfS9HSEtaKiWSlJFlSjoy3_Qm7TkkuNG6VbyTlL6hzrYHswWefnXbaLmslhpOykUK9TuP1Q5fks0jbBFfn-huV1wOSFmCHceKTFbQUwpiNkKYraCFP7F38Hc0b8bwX8BN2C5Jw</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Wu, Chengjiang</creator><creator>Zhao, Yangjing</creator><creator>Lin, Yu</creator><creator>Yang, Xinxin</creator><creator>Yan, Meina</creator><creator>Min, Yujiao</creator><creator>Pan, Zihui</creator><creator>Xia, Sheng</creator><creator>Shao, Qixiang</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20180301</creationdate><title>Bioinformatics analysis of differentially expressed gene profiles associated with systemic lupus erythematosus</title><author>Wu, Chengjiang ; Zhao, Yangjing ; Lin, Yu ; Yang, Xinxin ; Yan, Meina ; Min, Yujiao ; Pan, Zihui ; Xia, Sheng ; Shao, Qixiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-9a6adbfca483a990c106a8901521ed3d3f29528d33e8b1765f7e8e137dcdb1533</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Antigen presentation</topic><topic>Antigen processing</topic><topic>Bioinformatics</topic><topic>Care and treatment</topic><topic>Computational biology</topic><topic>Datasets</topic><topic>Development and progression</topic><topic>Disease</topic><topic>DNA helicase</topic><topic>DNA microarrays</topic><topic>DNA sequencing</topic><topic>Dynamin</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Genomes</topic><topic>Genotypes</topic><topic>Guanosine triphosphatases</topic><topic>Health aspects</topic><topic>Immune system</topic><topic>Immunoglobulin A</topic><topic>Innovations</topic><topic>Interferon regulatory factor</topic><topic>Interferon regulatory factor 7</topic><topic>Intestine</topic><topic>Lupus</topic><topic>Next-generation sequencing</topic><topic>Protein interaction</topic><topic>Proteins</topic><topic>Signal transduction</topic><topic>Studies</topic><topic>Systemic lupus erythematosus</topic><topic>Toll-like receptors</topic><topic>Transcription</topic><topic>Ubiquitin</topic><toplevel>online_resources</toplevel><creatorcontrib>Wu, Chengjiang</creatorcontrib><creatorcontrib>Zhao, Yangjing</creatorcontrib><creatorcontrib>Lin, Yu</creatorcontrib><creatorcontrib>Yang, Xinxin</creatorcontrib><creatorcontrib>Yan, Meina</creatorcontrib><creatorcontrib>Min, Yujiao</creatorcontrib><creatorcontrib>Pan, Zihui</creatorcontrib><creatorcontrib>Xia, Sheng</creatorcontrib><creatorcontrib>Shao, Qixiang</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wu, Chengjiang</au><au>Zhao, Yangjing</au><au>Lin, Yu</au><au>Yang, Xinxin</au><au>Yan, Meina</au><au>Min, Yujiao</au><au>Pan, Zihui</au><au>Xia, Sheng</au><au>Shao, Qixiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Bioinformatics analysis of differentially expressed gene profiles associated with systemic lupus erythematosus</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>17</volume><issue>3</issue><spage>3591</spage><epage>3598</epage><pages>3591-3598</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>DNA microarray and high-throughput sequencing have been widely used to identify the differentially expressed genes (DEGs) in systemic lupus erythematosus (SLE). However, the big data from gene microarrays are also challenging to work with in terms of analysis and processing. The presents study combined data from the microarray expression profile (GSE65391) and bioinformatics analysis to identify the key genes and cellular pathways in SLE. Gene ontology (GO) and cellular pathway enrichment analyses of DEGs were performed to investigate significantly enriched pathways. A protein‑protein interaction network was constructed to determine the key genes in the occurrence and development of SLE. A total of 310 DEGs were identified in SLE, including 193 upregulated genes and 117 downregulated genes. GO analysis revealed that the most significant biological process of DEGs was immune system process. Kyoto Encyclopedia of Genes and Genome pathway analysis showed that these DEGs were enriched in signaling pathways associated with the immune system, including the RIG‑I‑like receptor signaling pathway, intestinal immune network for IgA production, antigen processing and presentation and the toll‑like receptor signaling pathway. The current study screened the top 10 genes with higher degrees as hub genes, which included 2'‑5'‑oligoadenylate synthetase 1, MX dynamin like GTPase 2, interferon induced protein with tetratricopeptide repeats 1, interferon regulatory factor 7, interferon induced with helicase C domain 1, signal transducer and activator of transcription 1, ISG15 ubiquitin‑like modifier, DExD/H‑box helicase 58, interferon induced protein with tetratricopeptide repeats 3 and 2'‑5'‑oligoadenylate synthetase 2. Module analysis revealed that these hub genes were also involved in the RIG‑I‑like receptor signaling, cytosolic DNA‑sensing, toll‑like receptor signaling and ribosome biogenesis pathways. In addition, these hub genes, from different probe sets, exhibited significant co‑expressed tendency in multi‑experiment microarray datasets (P<0.01). In conclusion, these key genes and cellular pathways may improve the current understanding of the underlying mechanism of development of SLE. These key genes may be potential biomarkers of diagnosis, therapy and prognosis for SLE.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29257335</pmid><doi>10.3892/mmr.2017.8293</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Antigen presentation Antigen processing Bioinformatics Care and treatment Computational biology Datasets Development and progression Disease DNA helicase DNA microarrays DNA sequencing Dynamin Gene expression Genetic aspects Genomes Genotypes Guanosine triphosphatases Health aspects Immune system Immunoglobulin A Innovations Interferon regulatory factor Interferon regulatory factor 7 Intestine Lupus Next-generation sequencing Protein interaction Proteins Signal transduction Studies Systemic lupus erythematosus Toll-like receptors Transcription Ubiquitin |
title | Bioinformatics analysis of differentially expressed gene profiles associated with systemic lupus erythematosus |
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