lncRNA MEG3 restrained the M1 polarization of microglia in acute spinal cord injury through the HuR/A20/NF‐κB axis
The M1 polarization of microglia and neuroinflammation restrict the treatment of acute spinal cord injury (ASCI), and long non‐coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) expression is lessened in ASCI. However, the function and mechanism of lncRNA MEG3 in the M1 polarization...
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| Veröffentlicht in: | Brain pathology (Zurich, Switzerland) Switzerland), 2022-09, Vol.32 (5), p.e13070-n/a |
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| creator | Zhou, Heng‐Jun Wang, Li‐Qing Zhan, Ren‐Ya Zheng, Xiu‐Jue Zheng, Jie‐Sheng |
| description | The M1 polarization of microglia and neuroinflammation restrict the treatment of acute spinal cord injury (ASCI), and long non‐coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) expression is lessened in ASCI. However, the function and mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI are unclear. The expressions of lncRNA MEG3 in ASCI mouse spinal cord tissues and lipopolysaccharide (LPS)‐treated primary microglia and BV2 cells were quantified through a quantitative real‐time polymerase chain reaction. In‐vitro assays were conducted to explore the function of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI. RNA degradation, RNA immunoprecipitation, RNA pull‐down, cycloheximide‐chase, and ubiquitination analyses were carried out to probe into the mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI. The lncRNA MEG3 expression was lessened in the ASCI mouse spinal cord tissues and LPS‐treated primary microglia and BV2 cells, and the overexpression of lncRNA MEG3 restrained the M1 polarization of microglia and the neuroinflammation by regulating the NF‐κB signaling pathway. For the investigation of the potential mechanism of such, the overexpression of lncRNA MEG3 restrained the M1 polarization of microglia through the HuR/A20/NF‐κB axis and boosted the motor function recovery and neuroinflammation relief in the mice with SCI. The overexpression of lncRNA MEG3 restrained the M1 polarization of microglia through the HuR/A20/NF‐κB axis.
A working model was used to reveal the underlying mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation. |
| doi_str_mv | 10.1111/bpa.13070 |
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A working model was used to reveal the underlying mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation.</description><identifier>ISSN: 1015-6305</identifier><identifier>EISSN: 1750-3639</identifier><identifier>DOI: 10.1111/bpa.13070</identifier><identifier>PMID: 35338543</identifier><language>eng</language><publisher>Switzerland: John Wiley & Sons, Inc</publisher><subject>acute spinal cord injury ; Cycloheximide ; Ethylenediaminetetraacetic acid ; Gene expression ; HuR protein ; HuR/A20/NF‐κB ; Immunoprecipitation ; Inflammation ; Lipopolysaccharides ; lncRNA MEG3 ; M1 polarization of microglia ; Microglia ; neuroinflammation ; Non-coding RNA ; Polarization ; Polymerase chain reaction ; Ribonucleic acid ; RNA ; Signal transduction ; Spinal cord injuries ; Ubiquitination</subject><ispartof>Brain pathology (Zurich, Switzerland), 2022-09, Vol.32 (5), p.e13070-n/a</ispartof><rights>2022 The Authors. published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology.</rights><rights>2022 The Authors. Brain Pathology published by John Wiley & Sons Ltd on behalf of International Society of Neuropathology.</rights><rights>COPYRIGHT 2022 John Wiley & Sons, Inc.</rights><rights>2022. This work is published 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.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c5100-5595ec0f1c7744ad640bec618b12b1a8521c0c0f4ed86c11b4adc988bd6500fa3</citedby><cites>FETCH-LOGICAL-c5100-5595ec0f1c7744ad640bec618b12b1a8521c0c0f4ed86c11b4adc988bd6500fa3</cites><orcidid>0000-0001-9411-2879</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9425005/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC9425005/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,1416,11561,27923,27924,45573,45574,46051,46475,53790,53792</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/35338543$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zhou, Heng‐Jun</creatorcontrib><creatorcontrib>Wang, Li‐Qing</creatorcontrib><creatorcontrib>Zhan, Ren‐Ya</creatorcontrib><creatorcontrib>Zheng, Xiu‐Jue</creatorcontrib><creatorcontrib>Zheng, Jie‐Sheng</creatorcontrib><title>lncRNA MEG3 restrained the M1 polarization of microglia in acute spinal cord injury through the HuR/A20/NF‐κB axis</title><title>Brain pathology (Zurich, Switzerland)</title><addtitle>Brain Pathol</addtitle><description>The M1 polarization of microglia and neuroinflammation restrict the treatment of acute spinal cord injury (ASCI), and long non‐coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) expression is lessened in ASCI. However, the function and mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI are unclear. The expressions of lncRNA MEG3 in ASCI mouse spinal cord tissues and lipopolysaccharide (LPS)‐treated primary microglia and BV2 cells were quantified through a quantitative real‐time polymerase chain reaction. In‐vitro assays were conducted to explore the function of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI. RNA degradation, RNA immunoprecipitation, RNA pull‐down, cycloheximide‐chase, and ubiquitination analyses were carried out to probe into the mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI. The lncRNA MEG3 expression was lessened in the ASCI mouse spinal cord tissues and LPS‐treated primary microglia and BV2 cells, and the overexpression of lncRNA MEG3 restrained the M1 polarization of microglia and the neuroinflammation by regulating the NF‐κB signaling pathway. For the investigation of the potential mechanism of such, the overexpression of lncRNA MEG3 restrained the M1 polarization of microglia through the HuR/A20/NF‐κB axis and boosted the motor function recovery and neuroinflammation relief in the mice with SCI. The overexpression of lncRNA MEG3 restrained the M1 polarization of microglia through the HuR/A20/NF‐κB axis.
A working model was used to reveal the underlying mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation.</description><subject>acute spinal cord injury</subject><subject>Cycloheximide</subject><subject>Ethylenediaminetetraacetic acid</subject><subject>Gene expression</subject><subject>HuR protein</subject><subject>HuR/A20/NF‐κB</subject><subject>Immunoprecipitation</subject><subject>Inflammation</subject><subject>Lipopolysaccharides</subject><subject>lncRNA MEG3</subject><subject>M1 polarization of microglia</subject><subject>Microglia</subject><subject>neuroinflammation</subject><subject>Non-coding RNA</subject><subject>Polarization</subject><subject>Polymerase chain reaction</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Signal transduction</subject><subject>Spinal cord injuries</subject><subject>Ubiquitination</subject><issn>1015-6305</issn><issn>1750-3639</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2022</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp1ks1u1DAQxyMEoqVw4AWQJS5wyO44_khyQUqrfiC1BVVwthzH2fUqa2_tDbCceASeh4fgIXgSpt1SKAL7YGvmN__RfGTZUwoTimfarvSEMijhXrZLSwE5k6y-j3-gIpcMxE72KKUFAK1lLR5mO0wwVgnOdrNx8ObivCFnh8eMRJvWUTtvO7KeW3JGySoMOrrPeu2CJ6EnS2dimA1OE-eJNuPakrRyXg_EhNihcTHGDQbHMM7m1yIn48W0KWB6fvTjy9fv3_aJ_uTS4-xBr4dkn9y8e9n7o8N3Byf56Zvj1wfNaW4EBciFqIU10FNTlpzrTnJorZG0amnRUl2JghpAP7ddJQ2lLTKmrqq2kwKg12wve7XVXY3t0nbGeqxvUKvoljpuVNBO3fV4N1ez8EHVvEAFgQIvbgRiuByxPWrpkrHDoL0NY1KF5BxAFoVE9Plf6CKMEVuDVAllWdaFqH5TMz1Y5XwfMK-5ElVNyYFTgSBSk39QeDuLEwje9g7tdwJebgNwPClF29_WSEFd7YjCHVHXO4Lssz-bckv-WgoEplvgI2bZ_F9J7b9ttpI_AQfsxQw</recordid><startdate>202209</startdate><enddate>202209</enddate><creator>Zhou, Heng‐Jun</creator><creator>Wang, Li‐Qing</creator><creator>Zhan, Ren‐Ya</creator><creator>Zheng, Xiu‐Jue</creator><creator>Zheng, Jie‐Sheng</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>JQ2</scope><scope>K7-</scope><scope>K9.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0S</scope><scope>M7P</scope><scope>M7S</scope><scope>P5Z</scope><scope>P62</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9411-2879</orcidid></search><sort><creationdate>202209</creationdate><title>lncRNA MEG3 restrained the M1 polarization of microglia in acute spinal cord injury through the HuR/A20/NF‐κB axis</title><author>Zhou, Heng‐Jun ; Wang, Li‐Qing ; Zhan, Ren‐Ya ; Zheng, Xiu‐Jue ; Zheng, Jie‐Sheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c5100-5595ec0f1c7744ad640bec618b12b1a8521c0c0f4ed86c11b4adc988bd6500fa3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2022</creationdate><topic>acute spinal cord injury</topic><topic>Cycloheximide</topic><topic>Ethylenediaminetetraacetic acid</topic><topic>Gene expression</topic><topic>HuR protein</topic><topic>HuR/A20/NF‐κB</topic><topic>Immunoprecipitation</topic><topic>Inflammation</topic><topic>Lipopolysaccharides</topic><topic>lncRNA MEG3</topic><topic>M1 polarization of microglia</topic><topic>Microglia</topic><topic>neuroinflammation</topic><topic>Non-coding RNA</topic><topic>Polarization</topic><topic>Polymerase chain reaction</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Signal transduction</topic><topic>Spinal cord injuries</topic><topic>Ubiquitination</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhou, Heng‐Jun</creatorcontrib><creatorcontrib>Wang, Li‐Qing</creatorcontrib><creatorcontrib>Zhan, Ren‐Ya</creatorcontrib><creatorcontrib>Zheng, Xiu‐Jue</creatorcontrib><creatorcontrib>Zheng, Jie‐Sheng</creatorcontrib><collection>Wiley Open Access</collection><collection>Wiley Free Archive</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>ProQuest 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 Computer Science Collection</collection><collection>Computer Science Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Engineering Collection</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Biological Science Database</collection><collection>ProQuest Engineering Database</collection><collection>ProQuest Advanced Technologies & Aerospace Database</collection><collection>ProQuest Advanced Technologies & Aerospace Collection</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>Engineering Collection</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Brain pathology (Zurich, Switzerland)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhou, Heng‐Jun</au><au>Wang, Li‐Qing</au><au>Zhan, Ren‐Ya</au><au>Zheng, Xiu‐Jue</au><au>Zheng, Jie‐Sheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>lncRNA MEG3 restrained the M1 polarization of microglia in acute spinal cord injury through the HuR/A20/NF‐κB axis</atitle><jtitle>Brain pathology (Zurich, Switzerland)</jtitle><addtitle>Brain Pathol</addtitle><date>2022-09</date><risdate>2022</risdate><volume>32</volume><issue>5</issue><spage>e13070</spage><epage>n/a</epage><pages>e13070-n/a</pages><issn>1015-6305</issn><eissn>1750-3639</eissn><abstract>The M1 polarization of microglia and neuroinflammation restrict the treatment of acute spinal cord injury (ASCI), and long non‐coding ribonucleic acid (lncRNA) maternally expressed gene 3 (MEG3) expression is lessened in ASCI. However, the function and mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI are unclear. The expressions of lncRNA MEG3 in ASCI mouse spinal cord tissues and lipopolysaccharide (LPS)‐treated primary microglia and BV2 cells were quantified through a quantitative real‐time polymerase chain reaction. In‐vitro assays were conducted to explore the function of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI. RNA degradation, RNA immunoprecipitation, RNA pull‐down, cycloheximide‐chase, and ubiquitination analyses were carried out to probe into the mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation in ASCI. The lncRNA MEG3 expression was lessened in the ASCI mouse spinal cord tissues and LPS‐treated primary microglia and BV2 cells, and the overexpression of lncRNA MEG3 restrained the M1 polarization of microglia and the neuroinflammation by regulating the NF‐κB signaling pathway. For the investigation of the potential mechanism of such, the overexpression of lncRNA MEG3 restrained the M1 polarization of microglia through the HuR/A20/NF‐κB axis and boosted the motor function recovery and neuroinflammation relief in the mice with SCI. The overexpression of lncRNA MEG3 restrained the M1 polarization of microglia through the HuR/A20/NF‐κB axis.
A working model was used to reveal the underlying mechanism of lncRNA MEG3 in the M1 polarization of microglia and neuroinflammation.</abstract><cop>Switzerland</cop><pub>John Wiley & Sons, Inc</pub><pmid>35338543</pmid><doi>10.1111/bpa.13070</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0001-9411-2879</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | acute spinal cord injury Cycloheximide Ethylenediaminetetraacetic acid Gene expression HuR protein HuR/A20/NF‐κB Immunoprecipitation Inflammation Lipopolysaccharides lncRNA MEG3 M1 polarization of microglia Microglia neuroinflammation Non-coding RNA Polarization Polymerase chain reaction Ribonucleic acid RNA Signal transduction Spinal cord injuries Ubiquitination |
| title | lncRNA MEG3 restrained the M1 polarization of microglia in acute spinal cord injury through the HuR/A20/NF‐κB axis |
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