Long non-coding RNA Snhg16 Lessens Ozone Curative Effect on Chronic Constriction Injury mice via microRNA-719/SCN1A axis
We investigated the function and molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (Snhg16) in modifying ozone treatment for neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI). Pain-related behavioral responses were evaluated using paw with...
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description | We investigated the function and molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (Snhg16) in modifying ozone treatment for neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI). Pain-related behavioral responses were evaluated using paw withdrawal threshold (PWT), paw lifting number (PLN), and paw withdrawal latency (PWL) tests. Interleukin (IL)-1β, IL-10, IL-6, and tumor necrosis factor-alpha (TNF-α) were measured by ELISA and qRT-PCR to evaluate neuroinflammation. qRT-PCR was performed to detect expressions of Snhg16, microRNA (miR)-719, sodium voltage-gated channel alpha subunit 1 (SCN1A), and inflammatory factors. Bioinformatics, dual-luciferase reporter assay, and RNA pull-down verified the underlying molecular mechanisms. Snhg16 expression increased in CCI mice. Snhg16 overexpression retarded the curative effect of ozone and induced NP. miR-719 was sponged by Snhg16. SCN1A was a target of miR-719. Inhibition of miR-719 markedly reversed the effects of Snhg16 on pain-related behavioral responses and neuroinflammation. Upregulation of SCN1A partly abrogated the effects of elevated miR-719 levels on the occurrence of NP. The findings demonstrate that lncRNA Snhg16 promotes NP progression in CCI mice by binding to miR-719 to increase SCN1A expression. The Snhg16/miR-719/SCN1A axis may influence the curative effects of ozone therapy in treating NP.
Research Highlights
Ozone inhibits CCI-induced pain.
Snhg16 expression is increased in CCI mice.
Snhg16 can directly bind with miR-719, which targets SCN1A.
Snhg16/miR-719/SCN1A axis regulates pain and neuroinflammation. |
doi_str_mv | 10.1007/s12033-023-00847-3 |
format | Article |
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Research Highlights
Ozone inhibits CCI-induced pain.
Snhg16 expression is increased in CCI mice.
Snhg16 can directly bind with miR-719, which targets SCN1A.
Snhg16/miR-719/SCN1A axis regulates pain and neuroinflammation.</description><identifier>ISSN: 1073-6085</identifier><identifier>ISSN: 1559-0305</identifier><identifier>EISSN: 1559-0305</identifier><identifier>DOI: 10.1007/s12033-023-00847-3</identifier><identifier>PMID: 37632673</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Biochemistry ; Bioinformatics ; Biological Techniques ; bioluminescence assay ; Biotechnology ; Cell Biology ; Channel gating ; Chemistry ; Chemistry and Materials Science ; Constrictions ; Disease Models, Animal ; Enzyme-linked immunosorbent assay ; Gene expression ; Gene Expression Regulation - drug effects ; genes ; Human Genetics ; Inflammation ; Injury prevention ; interleukin-10 ; interleukin-6 ; Latency ; Male ; Mice ; Mice, Inbred C57BL ; microRNA ; MicroRNAs ; MicroRNAs - genetics ; miRNA ; Molecular modelling ; Neuralgia ; Neuralgia - drug therapy ; Neuralgia - genetics ; Neuralgia - metabolism ; Non-coding RNA ; Nucleoli ; Original Paper ; Ozonation ; Ozone ; Ozone - pharmacology ; Pain ; Polymerase chain reaction ; Protein Science ; Ribonucleic acid ; RNA ; RNA, Long Noncoding - genetics ; snoRNA ; sodium ; Sodium channels (voltage-gated) ; therapeutics ; tumor necrosis factor-alpha ; Tumor necrosis factor-TNF ; Tumor necrosis factor-α</subject><ispartof>Molecular biotechnology, 2024-09, Vol.66 (9), p.2273-2286</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c359t-5d5c4b3ff931d2dd9ee87ff2df25f3a2691f0bd55869a119c1135414211e67323</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s12033-023-00847-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s12033-023-00847-3$$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/37632673$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yue, Jianning</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Zhao, Wenxing</creatorcontrib><creatorcontrib>Wu, Baishan</creatorcontrib><creatorcontrib>Ni, Jiaxiang</creatorcontrib><title>Long non-coding RNA Snhg16 Lessens Ozone Curative Effect on Chronic Constriction Injury mice via microRNA-719/SCN1A axis</title><title>Molecular biotechnology</title><addtitle>Mol Biotechnol</addtitle><addtitle>Mol Biotechnol</addtitle><description>We investigated the function and molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (Snhg16) in modifying ozone treatment for neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI). Pain-related behavioral responses were evaluated using paw withdrawal threshold (PWT), paw lifting number (PLN), and paw withdrawal latency (PWL) tests. Interleukin (IL)-1β, IL-10, IL-6, and tumor necrosis factor-alpha (TNF-α) were measured by ELISA and qRT-PCR to evaluate neuroinflammation. qRT-PCR was performed to detect expressions of Snhg16, microRNA (miR)-719, sodium voltage-gated channel alpha subunit 1 (SCN1A), and inflammatory factors. Bioinformatics, dual-luciferase reporter assay, and RNA pull-down verified the underlying molecular mechanisms. Snhg16 expression increased in CCI mice. Snhg16 overexpression retarded the curative effect of ozone and induced NP. miR-719 was sponged by Snhg16. SCN1A was a target of miR-719. Inhibition of miR-719 markedly reversed the effects of Snhg16 on pain-related behavioral responses and neuroinflammation. Upregulation of SCN1A partly abrogated the effects of elevated miR-719 levels on the occurrence of NP. The findings demonstrate that lncRNA Snhg16 promotes NP progression in CCI mice by binding to miR-719 to increase SCN1A expression. The Snhg16/miR-719/SCN1A axis may influence the curative effects of ozone therapy in treating NP.
Research Highlights
Ozone inhibits CCI-induced pain.
Snhg16 expression is increased in CCI mice.
Snhg16 can directly bind with miR-719, which targets SCN1A.
Snhg16/miR-719/SCN1A axis regulates pain and neuroinflammation.</description><subject>Animals</subject><subject>Biochemistry</subject><subject>Bioinformatics</subject><subject>Biological Techniques</subject><subject>bioluminescence assay</subject><subject>Biotechnology</subject><subject>Cell Biology</subject><subject>Channel gating</subject><subject>Chemistry</subject><subject>Chemistry and Materials Science</subject><subject>Constrictions</subject><subject>Disease Models, Animal</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Gene expression</subject><subject>Gene Expression Regulation - drug effects</subject><subject>genes</subject><subject>Human Genetics</subject><subject>Inflammation</subject><subject>Injury prevention</subject><subject>interleukin-10</subject><subject>interleukin-6</subject><subject>Latency</subject><subject>Male</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>microRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>Neuralgia</subject><subject>Neuralgia - drug therapy</subject><subject>Neuralgia - genetics</subject><subject>Neuralgia - metabolism</subject><subject>Non-coding RNA</subject><subject>Nucleoli</subject><subject>Original Paper</subject><subject>Ozonation</subject><subject>Ozone</subject><subject>Ozone - pharmacology</subject><subject>Pain</subject><subject>Polymerase chain reaction</subject><subject>Protein Science</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>RNA, Long Noncoding - genetics</subject><subject>snoRNA</subject><subject>sodium</subject><subject>Sodium channels (voltage-gated)</subject><subject>therapeutics</subject><subject>tumor necrosis factor-alpha</subject><subject>Tumor necrosis factor-TNF</subject><subject>Tumor necrosis factor-α</subject><issn>1073-6085</issn><issn>1559-0305</issn><issn>1559-0305</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkcFPHCEUxompqdb2H_DQkPTSC8rjDTPDcTNRa7LRpOqZzDKwstkFCzNG-9eLrrZJD_ZA-AK_9z0eHyGHwI-A8-Y4g-CIjIuyeFs1DHfIPkipGEcuPxTNG2Q1b-Ue-ZTzinMBssKPZA-bGkXd4D55mMewpCEGZuLgi_x5MaNX4XYJNZ3bnG3I9PJ3DJZ2U-pHf2_piXPWjDQG2t2mGLyhXQx5TN6Mvhyeh9WUHunGG0vvff8sUiyurAF1fNVdwIz2Dz5_JruuX2f75XU_IDenJ9fdDza_PDvvZnNmUKqRyUGaaoHOKYRBDIOytm2cE4MT0mEvagWOLwYp21r1AMoAoKygEgC2DCjwgHzf-t6l-GuyedQbn41dr_tg45Q1gsQWBRT4f6hoZdNKrIUq6Ld_0FWcUiiDFEOuZHnPS2-xpcoP5Jys03fJb_r0qIHr5wj1NkJdItQvEWosRV9frafFxg5_St4yKwBugVyuwtKmv73fsX0CP-6jVg</recordid><startdate>20240901</startdate><enddate>20240901</enddate><creator>Yue, Jianning</creator><creator>Wang, Qi</creator><creator>Zhao, Wenxing</creator><creator>Wu, Baishan</creator><creator>Ni, Jiaxiang</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7U9</scope><scope>8FD</scope><scope>C1K</scope><scope>FR3</scope><scope>H94</scope><scope>K9.</scope><scope>M7N</scope><scope>P64</scope><scope>7X8</scope><scope>7S9</scope><scope>L.6</scope></search><sort><creationdate>20240901</creationdate><title>Long non-coding RNA Snhg16 Lessens Ozone Curative Effect on Chronic Constriction Injury mice via microRNA-719/SCN1A axis</title><author>Yue, Jianning ; Wang, Qi ; Zhao, Wenxing ; Wu, Baishan ; Ni, Jiaxiang</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c359t-5d5c4b3ff931d2dd9ee87ff2df25f3a2691f0bd55869a119c1135414211e67323</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Animals</topic><topic>Biochemistry</topic><topic>Bioinformatics</topic><topic>Biological Techniques</topic><topic>bioluminescence assay</topic><topic>Biotechnology</topic><topic>Cell Biology</topic><topic>Channel gating</topic><topic>Chemistry</topic><topic>Chemistry and Materials Science</topic><topic>Constrictions</topic><topic>Disease Models, Animal</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Gene expression</topic><topic>Gene Expression Regulation - drug effects</topic><topic>genes</topic><topic>Human Genetics</topic><topic>Inflammation</topic><topic>Injury prevention</topic><topic>interleukin-10</topic><topic>interleukin-6</topic><topic>Latency</topic><topic>Male</topic><topic>Mice</topic><topic>Mice, Inbred C57BL</topic><topic>microRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>miRNA</topic><topic>Molecular modelling</topic><topic>Neuralgia</topic><topic>Neuralgia - drug therapy</topic><topic>Neuralgia - genetics</topic><topic>Neuralgia - metabolism</topic><topic>Non-coding RNA</topic><topic>Nucleoli</topic><topic>Original Paper</topic><topic>Ozonation</topic><topic>Ozone</topic><topic>Ozone - pharmacology</topic><topic>Pain</topic><topic>Polymerase chain reaction</topic><topic>Protein Science</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>RNA, Long Noncoding - genetics</topic><topic>snoRNA</topic><topic>sodium</topic><topic>Sodium channels (voltage-gated)</topic><topic>therapeutics</topic><topic>tumor necrosis factor-alpha</topic><topic>Tumor necrosis factor-TNF</topic><topic>Tumor necrosis factor-α</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Yue, Jianning</creatorcontrib><creatorcontrib>Wang, Qi</creatorcontrib><creatorcontrib>Zhao, Wenxing</creatorcontrib><creatorcontrib>Wu, Baishan</creatorcontrib><creatorcontrib>Ni, Jiaxiang</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Technology Research Database</collection><collection>Environmental Sciences and Pollution Management</collection><collection>Engineering Research Database</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>MEDLINE - Academic</collection><collection>AGRICOLA</collection><collection>AGRICOLA - Academic</collection><jtitle>Molecular biotechnology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yue, Jianning</au><au>Wang, Qi</au><au>Zhao, Wenxing</au><au>Wu, Baishan</au><au>Ni, Jiaxiang</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long non-coding RNA Snhg16 Lessens Ozone Curative Effect on Chronic Constriction Injury mice via microRNA-719/SCN1A axis</atitle><jtitle>Molecular biotechnology</jtitle><stitle>Mol Biotechnol</stitle><addtitle>Mol Biotechnol</addtitle><date>2024-09-01</date><risdate>2024</risdate><volume>66</volume><issue>9</issue><spage>2273</spage><epage>2286</epage><pages>2273-2286</pages><issn>1073-6085</issn><issn>1559-0305</issn><eissn>1559-0305</eissn><abstract>We investigated the function and molecular mechanism of long non-coding RNA (lncRNA) small nucleolar RNA host gene 16 (Snhg16) in modifying ozone treatment for neuropathic pain (NP) in a mouse model of chronic constriction injury (CCI). Pain-related behavioral responses were evaluated using paw withdrawal threshold (PWT), paw lifting number (PLN), and paw withdrawal latency (PWL) tests. Interleukin (IL)-1β, IL-10, IL-6, and tumor necrosis factor-alpha (TNF-α) were measured by ELISA and qRT-PCR to evaluate neuroinflammation. qRT-PCR was performed to detect expressions of Snhg16, microRNA (miR)-719, sodium voltage-gated channel alpha subunit 1 (SCN1A), and inflammatory factors. Bioinformatics, dual-luciferase reporter assay, and RNA pull-down verified the underlying molecular mechanisms. Snhg16 expression increased in CCI mice. Snhg16 overexpression retarded the curative effect of ozone and induced NP. miR-719 was sponged by Snhg16. SCN1A was a target of miR-719. Inhibition of miR-719 markedly reversed the effects of Snhg16 on pain-related behavioral responses and neuroinflammation. Upregulation of SCN1A partly abrogated the effects of elevated miR-719 levels on the occurrence of NP. The findings demonstrate that lncRNA Snhg16 promotes NP progression in CCI mice by binding to miR-719 to increase SCN1A expression. The Snhg16/miR-719/SCN1A axis may influence the curative effects of ozone therapy in treating NP.
Research Highlights
Ozone inhibits CCI-induced pain.
Snhg16 expression is increased in CCI mice.
Snhg16 can directly bind with miR-719, which targets SCN1A.
Snhg16/miR-719/SCN1A axis regulates pain and neuroinflammation.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37632673</pmid><doi>10.1007/s12033-023-00847-3</doi><tpages>14</tpages></addata></record> |
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subjects | Animals Biochemistry Bioinformatics Biological Techniques bioluminescence assay Biotechnology Cell Biology Channel gating Chemistry Chemistry and Materials Science Constrictions Disease Models, Animal Enzyme-linked immunosorbent assay Gene expression Gene Expression Regulation - drug effects genes Human Genetics Inflammation Injury prevention interleukin-10 interleukin-6 Latency Male Mice Mice, Inbred C57BL microRNA MicroRNAs MicroRNAs - genetics miRNA Molecular modelling Neuralgia Neuralgia - drug therapy Neuralgia - genetics Neuralgia - metabolism Non-coding RNA Nucleoli Original Paper Ozonation Ozone Ozone - pharmacology Pain Polymerase chain reaction Protein Science Ribonucleic acid RNA RNA, Long Noncoding - genetics snoRNA sodium Sodium channels (voltage-gated) therapeutics tumor necrosis factor-alpha Tumor necrosis factor-TNF Tumor necrosis factor-α |
title | Long non-coding RNA Snhg16 Lessens Ozone Curative Effect on Chronic Constriction Injury mice via microRNA-719/SCN1A axis |
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