LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3
LINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose depriva...
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| Veröffentlicht in: | Human cell : official journal of Human Cell Research Society 2021-07, Vol.34 (4), p.1114-1122 |
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| creator | Zhu, Jiaying Zhu, Zhu Ren, Yipin Dong, Yukang Li, Yaqi Yang, Xiulin |
| description | LINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke. |
| doi_str_mv | 10.1007/s13577-021-00527-x |
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However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke.</description><identifier>ISSN: 1749-0774</identifier><identifier>ISSN: 0914-7470</identifier><identifier>EISSN: 1749-0774</identifier><identifier>DOI: 10.1007/s13577-021-00527-x</identifier><identifier>PMID: 33830473</identifier><language>eng</language><publisher>Singapore: Springer Singapore</publisher><subject>Animal models ; Apoptosis ; Biomedical and Life Sciences ; Brain injury ; Cell Biology ; Cell culture ; Cell proliferation ; Cerebral blood flow ; Gynecology ; Ischemia ; Janus kinase 2 ; Life Sciences ; mRNA ; NF-κB protein ; Nuclear transport ; Oncology ; Reperfusion ; Reproductive Medicine ; Research Article ; Stat3 protein ; Stem Cells ; Surgery</subject><ispartof>Human cell : official journal of Human Cell Research Society, 2021-07, Vol.34 (4), p.1114-1122</ispartof><rights>The Author(s) 2021</rights><rights>The Author(s) 2021. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). 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However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. In conclusion, our data suggest that shLINGO-1 attenuated ischemic injury by negatively regulating NF-KB and JAK2/STAT3 pathways, highlighting a novel therapeutic target for ischemic stroke.</description><subject>Animal models</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Brain injury</subject><subject>Cell Biology</subject><subject>Cell culture</subject><subject>Cell proliferation</subject><subject>Cerebral blood flow</subject><subject>Gynecology</subject><subject>Ischemia</subject><subject>Janus kinase 2</subject><subject>Life Sciences</subject><subject>mRNA</subject><subject>NF-κB protein</subject><subject>Nuclear transport</subject><subject>Oncology</subject><subject>Reperfusion</subject><subject>Reproductive Medicine</subject><subject>Research Article</subject><subject>Stat3 protein</subject><subject>Stem Cells</subject><subject>Surgery</subject><issn>1749-0774</issn><issn>0914-7470</issn><issn>1749-0774</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><recordid>eNp9kcFuEzEURS0EoqXlB1ggS2zYmNhjezyzQQoVLYUolUpYW7bjyThK7NT2VA2fxkfwTThNKaWLbuwn3fOu3_MF4A3BHwjGYpQI5UIgXBGEMa8EunkGDolgLcJCsOcP6gPwKqUlxoyzunoJDihtKGaCHoKfk_Pp2QUiMPWX0zHcxJCtyQnm3kIdlfNQLcqZMnTJ9Hbt1CjajY3dkFzw0PnlELdQb0vVO-2y84vbXmWyu1Z5x4QOTk_R71-foPJz-HX8rRp9n41n9Bi86NQq2dd39xH4cfp5dvIFTS7Ozk_GE2RY22Q0n7esa2rCsK6NILiijbCsKRonrWnrWlBrdCcwt7gT2jaEMaJqqzQnutUtPQIf976bQa_t3Fifo1rJTXRrFbcyKCf_V7zr5SJcy4a0QpCdwfs7gxiuBpuyXJfPsKuV8jYMSVa8TMVLFKyg7x6hyzBEX9YrFMOU1xjTQlV7ysSQUrTd_TAEy120ch-tLNHK22jlTWl6-3CN-5a_WRaA7oFUJL-w8d_bT9j-AYrNr5Q</recordid><startdate>20210701</startdate><enddate>20210701</enddate><creator>Zhu, Jiaying</creator><creator>Zhu, Zhu</creator><creator>Ren, Yipin</creator><creator>Dong, Yukang</creator><creator>Li, Yaqi</creator><creator>Yang, Xiulin</creator><general>Springer Singapore</general><general>Springer Nature B.V</general><scope>C6C</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-7464-3832</orcidid></search><sort><creationdate>20210701</creationdate><title>LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3</title><author>Zhu, Jiaying ; Zhu, Zhu ; Ren, Yipin ; Dong, Yukang ; Li, Yaqi ; Yang, Xiulin</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c498t-dd94f86140b6c7102387e48498519c96673ecbf705e0f7be81441a6eab51b9b93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animal models</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Brain injury</topic><topic>Cell Biology</topic><topic>Cell culture</topic><topic>Cell proliferation</topic><topic>Cerebral blood flow</topic><topic>Gynecology</topic><topic>Ischemia</topic><topic>Janus kinase 2</topic><topic>Life Sciences</topic><topic>mRNA</topic><topic>NF-κB protein</topic><topic>Nuclear transport</topic><topic>Oncology</topic><topic>Reperfusion</topic><topic>Reproductive Medicine</topic><topic>Research Article</topic><topic>Stat3 protein</topic><topic>Stem Cells</topic><topic>Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zhu, Jiaying</creatorcontrib><creatorcontrib>Zhu, Zhu</creatorcontrib><creatorcontrib>Ren, Yipin</creatorcontrib><creatorcontrib>Dong, Yukang</creatorcontrib><creatorcontrib>Li, Yaqi</creatorcontrib><creatorcontrib>Yang, Xiulin</creatorcontrib><collection>SpringerOpen</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Human cell : official journal of Human Cell Research Society</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zhu, Jiaying</au><au>Zhu, Zhu</au><au>Ren, Yipin</au><au>Dong, Yukang</au><au>Li, Yaqi</au><au>Yang, Xiulin</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3</atitle><jtitle>Human cell : official journal of Human Cell Research Society</jtitle><stitle>Human Cell</stitle><addtitle>Hum Cell</addtitle><date>2021-07-01</date><risdate>2021</risdate><volume>34</volume><issue>4</issue><spage>1114</spage><epage>1122</epage><pages>1114-1122</pages><issn>1749-0774</issn><issn>0914-7470</issn><eissn>1749-0774</eissn><abstract>LINGO-1 may be involved in the pathogenesis of cerebral ischemia. However, its biological function and underlying molecular mechanism in cerebral ischemia remain to be further defined. In our study, middle cerebral artery occlusion/reperfusion (MACO/R) mice model and HT22 cell oxygen–glucose deprivation/reperfusion (OGD/R) were established to simulate the pathological process of cerebral ischemia in vivo and in vitro and to detect the relevant mechanism. We found that LINGO-1 mRNA and protein were upregulated in mice and cell models. Down-regulation LINGO-1 improved the neurological symptoms and reduced pathological changes and the infarct size of the mice after MACO/R. In addition, LINGO-1 interference alleviated apoptosis and promoted cell proliferation in HT22 of OGD/R. Moreover, down-regulation of LINGO-1 proved to inhibit nuclear translocation of p-NF-κB and reduce the expression level of p-JAK2 and p-STAT3. 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| subjects | Animal models Apoptosis Biomedical and Life Sciences Brain injury Cell Biology Cell culture Cell proliferation Cerebral blood flow Gynecology Ischemia Janus kinase 2 Life Sciences mRNA NF-κB protein Nuclear transport Oncology Reperfusion Reproductive Medicine Research Article Stat3 protein Stem Cells Surgery |
| title | LINGO-1 shRNA protects the brain against ischemia/reperfusion injury by inhibiting the activation of NF-κB and JAK2/STAT3 |
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