Whole Genomic DNA Methylation Profiling of CpG Sites in Promoter Regions of Dorsal Root Ganglion in Diabetic Neuropathic Pain Mice
DNA methylation and demethylation play an important role in neuropathic pain. In general, DNA methylation of CpG sites in the promoter region impedes gene expression, whereas DNA demethylation contributes to gene expression. Here, we evaluated the methylation status of CpG sites in genomic DNA promo...
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| Veröffentlicht in: | Journal of molecular neuroscience 2021-12, Vol.71 (12), p.2558-2565 |
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| creator | Chen, Wen Lan, Ting Sun, Qingyu Zhang, Yurui Shen, Danmin Hu, Tingting Liu, Jing Chong, Yingzi Wang, Peipei Li, Qian Cui, Weihua Yang, Fei |
| description | DNA methylation and demethylation play an important role in neuropathic pain. In general, DNA methylation of CpG sites in the promoter region impedes gene expression, whereas DNA demethylation contributes to gene expression. Here, we evaluated the methylation status of CpG sites in genomic DNA promoter regions in dorsal root ganglions (DRGs) of diabetic neuropathic pain (DNP) mice. In our research, streptozotocin (STZ) was intraperitoneally injected into mice to construct DNP models. The DNP mice showed higher fasting blood glucose (above 11.1 mmol/L), lower body weight, and mechanical allodynia than control mice. Whole-genome bisulfite sequencing (WGBS) revealed an altered methylation pattern in CpG sites in the DNA promoter regions in DRGs of DNP mice. The results showed 376 promoter regions with hypermethylated CpG sites and 336 promoter regions with hypomethylated CpG sites. In addition, our data indicated that altered DNA methylation occurs primarily on CpG sites in DNA promoter regions. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that differentially methylated CpG sites annotated genes were involved in activities of the nervous and sensory systems. Enrichment analysis indicated that genes in these pathways contributed to diabetes or pain. In conclusion, our study enriched the role of DNA methylation in DNP. |
| doi_str_mv | 10.1007/s12031-021-01847-1 |
| format | Article |
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In general, DNA methylation of CpG sites in the promoter region impedes gene expression, whereas DNA demethylation contributes to gene expression. Here, we evaluated the methylation status of CpG sites in genomic DNA promoter regions in dorsal root ganglions (DRGs) of diabetic neuropathic pain (DNP) mice. In our research, streptozotocin (STZ) was intraperitoneally injected into mice to construct DNP models. The DNP mice showed higher fasting blood glucose (above 11.1 mmol/L), lower body weight, and mechanical allodynia than control mice. Whole-genome bisulfite sequencing (WGBS) revealed an altered methylation pattern in CpG sites in the DNA promoter regions in DRGs of DNP mice. The results showed 376 promoter regions with hypermethylated CpG sites and 336 promoter regions with hypomethylated CpG sites. In addition, our data indicated that altered DNA methylation occurs primarily on CpG sites in DNA promoter regions. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that differentially methylated CpG sites annotated genes were involved in activities of the nervous and sensory systems. Enrichment analysis indicated that genes in these pathways contributed to diabetes or pain. In conclusion, our study enriched the role of DNA methylation in DNP.</description><identifier>ISSN: 0895-8696</identifier><identifier>EISSN: 1559-1166</identifier><identifier>DOI: 10.1007/s12031-021-01847-1</identifier><identifier>PMID: 33950354</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animal models ; Animals ; Biomedical and Life Sciences ; Biomedicine ; Bisulfite ; Body weight ; Cell Biology ; CpG Islands ; Demethylation ; Deoxyribonucleic acid ; Diabetes ; Diabetes mellitus ; Diabetic Neuropathies - genetics ; Diabetic neuropathy ; DNA ; DNA fingerprinting ; DNA Methylation ; Dorsal root ganglia ; Encyclopedias ; Ganglia, Spinal - metabolism ; Gene expression ; Gene sequencing ; Genes ; Genomes ; Genomics ; Mice ; Mice, Inbred C57BL ; Neuralgia - genetics ; Neurochemistry ; Neurology ; Neurosciences ; Pain ; Pain perception ; Promoter Regions, Genetic ; Proteomics ; Sensory evaluation ; Sensory systems ; Streptozocin ; Whole Genome Sequencing</subject><ispartof>Journal of molecular neuroscience, 2021-12, Vol.71 (12), p.2558-2565</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-64763c9178bc19f80d792c450128ef22b0da2c37235f086610352f98bbdb33863</citedby><cites>FETCH-LOGICAL-c375t-64763c9178bc19f80d792c450128ef22b0da2c37235f086610352f98bbdb33863</cites><orcidid>0000-0003-3122-2960</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12031-021-01847-1$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12031-021-01847-1$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/33950354$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Chen, Wen</creatorcontrib><creatorcontrib>Lan, Ting</creatorcontrib><creatorcontrib>Sun, Qingyu</creatorcontrib><creatorcontrib>Zhang, Yurui</creatorcontrib><creatorcontrib>Shen, Danmin</creatorcontrib><creatorcontrib>Hu, Tingting</creatorcontrib><creatorcontrib>Liu, Jing</creatorcontrib><creatorcontrib>Chong, Yingzi</creatorcontrib><creatorcontrib>Wang, Peipei</creatorcontrib><creatorcontrib>Li, Qian</creatorcontrib><creatorcontrib>Cui, Weihua</creatorcontrib><creatorcontrib>Yang, Fei</creatorcontrib><title>Whole Genomic DNA Methylation Profiling of CpG Sites in Promoter Regions of Dorsal Root Ganglion in Diabetic Neuropathic Pain Mice</title><title>Journal of molecular neuroscience</title><addtitle>J Mol Neurosci</addtitle><addtitle>J Mol Neurosci</addtitle><description>DNA methylation and demethylation play an important role in neuropathic pain. In general, DNA methylation of CpG sites in the promoter region impedes gene expression, whereas DNA demethylation contributes to gene expression. Here, we evaluated the methylation status of CpG sites in genomic DNA promoter regions in dorsal root ganglions (DRGs) of diabetic neuropathic pain (DNP) mice. In our research, streptozotocin (STZ) was intraperitoneally injected into mice to construct DNP models. The DNP mice showed higher fasting blood glucose (above 11.1 mmol/L), lower body weight, and mechanical allodynia than control mice. Whole-genome bisulfite sequencing (WGBS) revealed an altered methylation pattern in CpG sites in the DNA promoter regions in DRGs of DNP mice. The results showed 376 promoter regions with hypermethylated CpG sites and 336 promoter regions with hypomethylated CpG sites. In addition, our data indicated that altered DNA methylation occurs primarily on CpG sites in DNA promoter regions. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that differentially methylated CpG sites annotated genes were involved in activities of the nervous and sensory systems. Enrichment analysis indicated that genes in these pathways contributed to diabetes or pain. In conclusion, our study enriched the role of DNA methylation in DNP.</description><subject>Animal models</subject><subject>Animals</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Bisulfite</subject><subject>Body weight</subject><subject>Cell Biology</subject><subject>CpG Islands</subject><subject>Demethylation</subject><subject>Deoxyribonucleic acid</subject><subject>Diabetes</subject><subject>Diabetes mellitus</subject><subject>Diabetic Neuropathies - genetics</subject><subject>Diabetic neuropathy</subject><subject>DNA</subject><subject>DNA fingerprinting</subject><subject>DNA Methylation</subject><subject>Dorsal root ganglia</subject><subject>Encyclopedias</subject><subject>Ganglia, Spinal - metabolism</subject><subject>Gene expression</subject><subject>Gene sequencing</subject><subject>Genes</subject><subject>Genomes</subject><subject>Genomics</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Neuralgia - genetics</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Pain</subject><subject>Pain perception</subject><subject>Promoter Regions, Genetic</subject><subject>Proteomics</subject><subject>Sensory evaluation</subject><subject>Sensory systems</subject><subject>Streptozocin</subject><subject>Whole Genome Sequencing</subject><issn>0895-8696</issn><issn>1559-1166</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kUtPGzEUha2qqAToH-gCWeqmmyl-jD32EiU0VOIR0VZdWp7JncRoZhxsz4Jtf3kdEkBiwcK6ls53z7XvQegLJd8pIdVZpIxwWhCWD1VlVdAPaEKF0AWlUn5EE6K0KJTU8hAdxXhPMllS9Qkdcq4F4aKcoH9_174DPIfB967Bs5tzfA1p_djZ5PyAF8G3rnPDCvsWTzdz_MsliNg9Kb1PEPAdrDIZt8DMh2g7fOd9wnM7rLqtRWZnztaQsv0NjMFvbFrn-8Jm5do1cIIOWttF-Lyvx-jPj4vf08vi6nb-c3p-VTS8EqmQZSV5o2ml6obqVpFlpVlTCkKZgpaxmiwtyyjjoiVKSpo_yFqt6npZc64kP0bfdr6b4B9GiMn0LjbQdXYAP0bDBGMlIVqxjH59g977MQz5dZnSSnHJJM0U21FN8DEGaM0muN6GR0OJ2SZkdgmZvHfzlJDZNp3urce6h-VLy3MkGeA7IGZpWEF4nf2O7X8ZmZm3</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Chen, Wen</creator><creator>Lan, Ting</creator><creator>Sun, Qingyu</creator><creator>Zhang, Yurui</creator><creator>Shen, Danmin</creator><creator>Hu, Tingting</creator><creator>Liu, Jing</creator><creator>Chong, Yingzi</creator><creator>Wang, Peipei</creator><creator>Li, Qian</creator><creator>Cui, Weihua</creator><creator>Yang, Fei</creator><general>Springer US</general><general>Springer Nature B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QL</scope><scope>7QR</scope><scope>7T7</scope><scope>7TK</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FD</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>M7N</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0003-3122-2960</orcidid></search><sort><creationdate>20211201</creationdate><title>Whole Genomic DNA Methylation Profiling of CpG Sites in Promoter Regions of Dorsal Root Ganglion in Diabetic Neuropathic Pain Mice</title><author>Chen, Wen ; Lan, Ting ; Sun, Qingyu ; Zhang, Yurui ; Shen, Danmin ; Hu, Tingting ; Liu, Jing ; Chong, Yingzi ; Wang, Peipei ; Li, Qian ; Cui, Weihua ; Yang, Fei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-64763c9178bc19f80d792c450128ef22b0da2c37235f086610352f98bbdb33863</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animal models</topic><topic>Animals</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Bisulfite</topic><topic>Body weight</topic><topic>Cell Biology</topic><topic>CpG Islands</topic><topic>Demethylation</topic><topic>Deoxyribonucleic acid</topic><topic>Diabetes</topic><topic>Diabetes mellitus</topic><topic>Diabetic Neuropathies - 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Academic</collection><jtitle>Journal of molecular neuroscience</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Chen, Wen</au><au>Lan, Ting</au><au>Sun, Qingyu</au><au>Zhang, Yurui</au><au>Shen, Danmin</au><au>Hu, Tingting</au><au>Liu, Jing</au><au>Chong, Yingzi</au><au>Wang, Peipei</au><au>Li, Qian</au><au>Cui, Weihua</au><au>Yang, Fei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Whole Genomic DNA Methylation Profiling of CpG Sites in Promoter Regions of Dorsal Root Ganglion in Diabetic Neuropathic Pain Mice</atitle><jtitle>Journal of molecular neuroscience</jtitle><stitle>J Mol Neurosci</stitle><addtitle>J Mol Neurosci</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>71</volume><issue>12</issue><spage>2558</spage><epage>2565</epage><pages>2558-2565</pages><issn>0895-8696</issn><eissn>1559-1166</eissn><abstract>DNA methylation and demethylation play an important role in neuropathic pain. In general, DNA methylation of CpG sites in the promoter region impedes gene expression, whereas DNA demethylation contributes to gene expression. Here, we evaluated the methylation status of CpG sites in genomic DNA promoter regions in dorsal root ganglions (DRGs) of diabetic neuropathic pain (DNP) mice. In our research, streptozotocin (STZ) was intraperitoneally injected into mice to construct DNP models. The DNP mice showed higher fasting blood glucose (above 11.1 mmol/L), lower body weight, and mechanical allodynia than control mice. Whole-genome bisulfite sequencing (WGBS) revealed an altered methylation pattern in CpG sites in the DNA promoter regions in DRGs of DNP mice. The results showed 376 promoter regions with hypermethylated CpG sites and 336 promoter regions with hypomethylated CpG sites. In addition, our data indicated that altered DNA methylation occurs primarily on CpG sites in DNA promoter regions. The Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis revealed that differentially methylated CpG sites annotated genes were involved in activities of the nervous and sensory systems. Enrichment analysis indicated that genes in these pathways contributed to diabetes or pain. In conclusion, our study enriched the role of DNA methylation in DNP.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>33950354</pmid><doi>10.1007/s12031-021-01847-1</doi><tpages>8</tpages><orcidid>https://orcid.org/0000-0003-3122-2960</orcidid></addata></record> |
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| subjects | Animal models Animals Biomedical and Life Sciences Biomedicine Bisulfite Body weight Cell Biology CpG Islands Demethylation Deoxyribonucleic acid Diabetes Diabetes mellitus Diabetic Neuropathies - genetics Diabetic neuropathy DNA DNA fingerprinting DNA Methylation Dorsal root ganglia Encyclopedias Ganglia, Spinal - metabolism Gene expression Gene sequencing Genes Genomes Genomics Mice Mice, Inbred C57BL Neuralgia - genetics Neurochemistry Neurology Neurosciences Pain Pain perception Promoter Regions, Genetic Proteomics Sensory evaluation Sensory systems Streptozocin Whole Genome Sequencing |
| title | Whole Genomic DNA Methylation Profiling of CpG Sites in Promoter Regions of Dorsal Root Ganglion in Diabetic Neuropathic Pain Mice |
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