Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13
•MiR-874-3p attenuated cerebral I/R induced rat brain tissue injury.•MiR-874-3p promoted proliferation and attenuated apoptosis in OGD/R-induced SH-SY5Y cells.•MiR-874-3p directly targets the 3′UTR of BMF and BCL2L13.•MiR-874-3p exerted protective roles against OGD/R-induced injury by downregulating...
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Veröffentlicht in: | Biomedicine & pharmacotherapy 2019-09, Vol.117, p.108941-108941, Article 108941 |
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description | •MiR-874-3p attenuated cerebral I/R induced rat brain tissue injury.•MiR-874-3p promoted proliferation and attenuated apoptosis in OGD/R-induced SH-SY5Y cells.•MiR-874-3p directly targets the 3′UTR of BMF and BCL2L13.•MiR-874-3p exerted protective roles against OGD/R-induced injury by downregulating BMF and BCL2L13.
Ischemic stroke represents a major cause of adult physical disability, which is triggered by cerebral artery occlusion induced blood flow blockage. MiR-874-3p has been reported to be down-regulated in the brain injury induced by ischemia-reperfusion (I/R), but the direct evidence associated with injury of I/R remains unknown. In this study, we found that miR-874-3p levels significantly decreased in rat I/R brain induced by middle cerebral artery occlusion/reperfusion (MCAO/R) and SH-SY5Y cells following oxygen-glucose deprivation and reperfusion (OGD/R) treatment. Upregulation of miR-874-3p reduced infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining, as well as increased proliferation and inhibited apoptosis in OGD/R induced SH-SY5Y cells by CCK-8, Edu staining and flow cytometry analysis. Mechanistically, bioinformatics analysis and luciferase reporter assay confirmed BCL-2-modifying factor (BMF) and Bcl-2 family protein Bcl-rambo (BCL2L13) were the direct targets of miR-874-3p. Furthermore, BMF or BCL2L13 knockdown also provided significant protection against OGD/R induced injury, while their overexpression reversed the protective effects of miR-874-3p on SH-SY5Y cells following OGD/R. In summary, our results suggest that miR-874-3p attenuated ischemic injury by negatively regulating BMF and BCL2L13, highlighting a novel therapeutic target for ischemic stroke. |
doi_str_mv | 10.1016/j.biopha.2019.108941 |
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Ischemic stroke represents a major cause of adult physical disability, which is triggered by cerebral artery occlusion induced blood flow blockage. MiR-874-3p has been reported to be down-regulated in the brain injury induced by ischemia-reperfusion (I/R), but the direct evidence associated with injury of I/R remains unknown. In this study, we found that miR-874-3p levels significantly decreased in rat I/R brain induced by middle cerebral artery occlusion/reperfusion (MCAO/R) and SH-SY5Y cells following oxygen-glucose deprivation and reperfusion (OGD/R) treatment. Upregulation of miR-874-3p reduced infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining, as well as increased proliferation and inhibited apoptosis in OGD/R induced SH-SY5Y cells by CCK-8, Edu staining and flow cytometry analysis. Mechanistically, bioinformatics analysis and luciferase reporter assay confirmed BCL-2-modifying factor (BMF) and Bcl-2 family protein Bcl-rambo (BCL2L13) were the direct targets of miR-874-3p. Furthermore, BMF or BCL2L13 knockdown also provided significant protection against OGD/R induced injury, while their overexpression reversed the protective effects of miR-874-3p on SH-SY5Y cells following OGD/R. In summary, our results suggest that miR-874-3p attenuated ischemic injury by negatively regulating BMF and BCL2L13, highlighting a novel therapeutic target for ischemic stroke.</description><identifier>ISSN: 0753-3322</identifier><identifier>EISSN: 1950-6007</identifier><identifier>DOI: 10.1016/j.biopha.2019.108941</identifier><identifier>PMID: 31200256</identifier><language>eng</language><publisher>France: Elsevier Masson SAS</publisher><subject>3' Untranslated Regions - genetics ; Adaptor Proteins, Signal Transducing - genetics ; Adaptor Proteins, Signal Transducing - metabolism ; Animals ; Apoptosis - genetics ; Base Sequence ; BCL2L13 ; BMF ; Brain Ischemia - complications ; Brain Ischemia - genetics ; Cell Line, Tumor ; Cell Proliferation ; Down-Regulation - genetics ; Glucose - deficiency ; Humans ; Ischemia-reperfusion ; Male ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miR-874-3p ; OGD/R ; Oxygen ; Proto-Oncogene Proteins c-bcl-2 - genetics ; Proto-Oncogene Proteins c-bcl-2 - metabolism ; Rats ; Reperfusion Injury - complications ; Reperfusion Injury - genetics ; Stroke ; Up-Regulation - genetics</subject><ispartof>Biomedicine & pharmacotherapy, 2019-09, Vol.117, p.108941-108941, Article 108941</ispartof><rights>2019 The Authors</rights><rights>Copyright © 2019 The Authors. Published by Elsevier Masson SAS.. All rights reserved.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c408t-9545cc1c349c4d03c02c29da49a54826eb7bba7736e98f7de2317dfa98e9d5013</citedby><cites>FETCH-LOGICAL-c408t-9545cc1c349c4d03c02c29da49a54826eb7bba7736e98f7de2317dfa98e9d5013</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.biopha.2019.108941$$EHTML$$P50$$Gelsevier$$Hfree_for_read</linktohtml><link.rule.ids>314,780,784,3548,27923,27924,45994</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31200256$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Jiang, Dongxiao</creatorcontrib><creatorcontrib>Sun, Xinhu</creatorcontrib><creatorcontrib>Wang, Shengwu</creatorcontrib><creatorcontrib>Man, Honghao</creatorcontrib><title>Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13</title><title>Biomedicine & pharmacotherapy</title><addtitle>Biomed Pharmacother</addtitle><description>•MiR-874-3p attenuated cerebral I/R induced rat brain tissue injury.•MiR-874-3p promoted proliferation and attenuated apoptosis in OGD/R-induced SH-SY5Y cells.•MiR-874-3p directly targets the 3′UTR of BMF and BCL2L13.•MiR-874-3p exerted protective roles against OGD/R-induced injury by downregulating BMF and BCL2L13.
Ischemic stroke represents a major cause of adult physical disability, which is triggered by cerebral artery occlusion induced blood flow blockage. MiR-874-3p has been reported to be down-regulated in the brain injury induced by ischemia-reperfusion (I/R), but the direct evidence associated with injury of I/R remains unknown. In this study, we found that miR-874-3p levels significantly decreased in rat I/R brain induced by middle cerebral artery occlusion/reperfusion (MCAO/R) and SH-SY5Y cells following oxygen-glucose deprivation and reperfusion (OGD/R) treatment. Upregulation of miR-874-3p reduced infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining, as well as increased proliferation and inhibited apoptosis in OGD/R induced SH-SY5Y cells by CCK-8, Edu staining and flow cytometry analysis. Mechanistically, bioinformatics analysis and luciferase reporter assay confirmed BCL-2-modifying factor (BMF) and Bcl-2 family protein Bcl-rambo (BCL2L13) were the direct targets of miR-874-3p. Furthermore, BMF or BCL2L13 knockdown also provided significant protection against OGD/R induced injury, while their overexpression reversed the protective effects of miR-874-3p on SH-SY5Y cells following OGD/R. In summary, our results suggest that miR-874-3p attenuated ischemic injury by negatively regulating BMF and BCL2L13, highlighting a novel therapeutic target for ischemic stroke.</description><subject>3' Untranslated Regions - genetics</subject><subject>Adaptor Proteins, Signal Transducing - genetics</subject><subject>Adaptor Proteins, Signal Transducing - metabolism</subject><subject>Animals</subject><subject>Apoptosis - genetics</subject><subject>Base Sequence</subject><subject>BCL2L13</subject><subject>BMF</subject><subject>Brain Ischemia - complications</subject><subject>Brain Ischemia - genetics</subject><subject>Cell Line, Tumor</subject><subject>Cell Proliferation</subject><subject>Down-Regulation - genetics</subject><subject>Glucose - deficiency</subject><subject>Humans</subject><subject>Ischemia-reperfusion</subject><subject>Male</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miR-874-3p</subject><subject>OGD/R</subject><subject>Oxygen</subject><subject>Proto-Oncogene Proteins c-bcl-2 - genetics</subject><subject>Proto-Oncogene Proteins c-bcl-2 - metabolism</subject><subject>Rats</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - genetics</subject><subject>Stroke</subject><subject>Up-Regulation - genetics</subject><issn>0753-3322</issn><issn>1950-6007</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kEtr3DAURkVpaCZp_0EJWnbjydXLtjaBZsgLJgRCsxaydD3R4FclOzD_Ph6cdpnVhcv57uMQ8pPBmgHLL_frKvTDq11zYHpulVqyL2TFtIIsByi-khUUSmRCcH5KzlLaA4DKRfmNnArGAbjKV6R_GSLupsaOoe9oX9M2PGdlITMxUI8uok2YqMOIVbQNDcm9YhvsZcQBYz2lYyp0-ykeaHWgPkR0Y3Ogo407HEO3o9ePt9R2nl5vtnzLxHdyUtsm4Y-Pek5ebm_-bO6z7dPdw-b3NnMSyjHTSirnmBNSO-lBOOCOa2-ltkqWPMeqqCpbFCJHXdaFRy5Y4WurS9ReARPn5Ncyd4j93wnTaNr5dmwa22E_JcO55EwpJvSMygV1sU8pYm2GGFobD4aBOao2e7OoNkfVZlE9xy4-NkxVi_5_6J_bGbhaAJz_fAsYTXIBO4eLJeP78PmGd22pkHQ</recordid><startdate>201909</startdate><enddate>201909</enddate><creator>Jiang, Dongxiao</creator><creator>Sun, Xinhu</creator><creator>Wang, Shengwu</creator><creator>Man, Honghao</creator><general>Elsevier Masson SAS</general><scope>6I.</scope><scope>AAFTH</scope><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>7X8</scope></search><sort><creationdate>201909</creationdate><title>Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13</title><author>Jiang, Dongxiao ; Sun, Xinhu ; Wang, Shengwu ; Man, Honghao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c408t-9545cc1c349c4d03c02c29da49a54826eb7bba7736e98f7de2317dfa98e9d5013</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>3' Untranslated Regions - genetics</topic><topic>Adaptor Proteins, Signal Transducing - genetics</topic><topic>Adaptor Proteins, Signal Transducing - metabolism</topic><topic>Animals</topic><topic>Apoptosis - genetics</topic><topic>Base Sequence</topic><topic>BCL2L13</topic><topic>BMF</topic><topic>Brain Ischemia - complications</topic><topic>Brain Ischemia - genetics</topic><topic>Cell Line, Tumor</topic><topic>Cell Proliferation</topic><topic>Down-Regulation - genetics</topic><topic>Glucose - deficiency</topic><topic>Humans</topic><topic>Ischemia-reperfusion</topic><topic>Male</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miR-874-3p</topic><topic>OGD/R</topic><topic>Oxygen</topic><topic>Proto-Oncogene Proteins c-bcl-2 - genetics</topic><topic>Proto-Oncogene Proteins c-bcl-2 - metabolism</topic><topic>Rats</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - genetics</topic><topic>Stroke</topic><topic>Up-Regulation - genetics</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Jiang, Dongxiao</creatorcontrib><creatorcontrib>Sun, Xinhu</creatorcontrib><creatorcontrib>Wang, Shengwu</creatorcontrib><creatorcontrib>Man, Honghao</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Biomedicine & pharmacotherapy</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Jiang, Dongxiao</au><au>Sun, Xinhu</au><au>Wang, Shengwu</au><au>Man, Honghao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13</atitle><jtitle>Biomedicine & pharmacotherapy</jtitle><addtitle>Biomed Pharmacother</addtitle><date>2019-09</date><risdate>2019</risdate><volume>117</volume><spage>108941</spage><epage>108941</epage><pages>108941-108941</pages><artnum>108941</artnum><issn>0753-3322</issn><eissn>1950-6007</eissn><abstract>•MiR-874-3p attenuated cerebral I/R induced rat brain tissue injury.•MiR-874-3p promoted proliferation and attenuated apoptosis in OGD/R-induced SH-SY5Y cells.•MiR-874-3p directly targets the 3′UTR of BMF and BCL2L13.•MiR-874-3p exerted protective roles against OGD/R-induced injury by downregulating BMF and BCL2L13.
Ischemic stroke represents a major cause of adult physical disability, which is triggered by cerebral artery occlusion induced blood flow blockage. MiR-874-3p has been reported to be down-regulated in the brain injury induced by ischemia-reperfusion (I/R), but the direct evidence associated with injury of I/R remains unknown. In this study, we found that miR-874-3p levels significantly decreased in rat I/R brain induced by middle cerebral artery occlusion/reperfusion (MCAO/R) and SH-SY5Y cells following oxygen-glucose deprivation and reperfusion (OGD/R) treatment. Upregulation of miR-874-3p reduced infarct volumes and cell apoptosis in the in vivo I/R stroke model using TTC and TUNEL staining, as well as increased proliferation and inhibited apoptosis in OGD/R induced SH-SY5Y cells by CCK-8, Edu staining and flow cytometry analysis. Mechanistically, bioinformatics analysis and luciferase reporter assay confirmed BCL-2-modifying factor (BMF) and Bcl-2 family protein Bcl-rambo (BCL2L13) were the direct targets of miR-874-3p. Furthermore, BMF or BCL2L13 knockdown also provided significant protection against OGD/R induced injury, while their overexpression reversed the protective effects of miR-874-3p on SH-SY5Y cells following OGD/R. In summary, our results suggest that miR-874-3p attenuated ischemic injury by negatively regulating BMF and BCL2L13, highlighting a novel therapeutic target for ischemic stroke.</abstract><cop>France</cop><pub>Elsevier Masson SAS</pub><pmid>31200256</pmid><doi>10.1016/j.biopha.2019.108941</doi><tpages>1</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 3' Untranslated Regions - genetics Adaptor Proteins, Signal Transducing - genetics Adaptor Proteins, Signal Transducing - metabolism Animals Apoptosis - genetics Base Sequence BCL2L13 BMF Brain Ischemia - complications Brain Ischemia - genetics Cell Line, Tumor Cell Proliferation Down-Regulation - genetics Glucose - deficiency Humans Ischemia-reperfusion Male MicroRNAs - genetics MicroRNAs - metabolism miR-874-3p OGD/R Oxygen Proto-Oncogene Proteins c-bcl-2 - genetics Proto-Oncogene Proteins c-bcl-2 - metabolism Rats Reperfusion Injury - complications Reperfusion Injury - genetics Stroke Up-Regulation - genetics |
title | Upregulation of miR-874-3p decreases cerebral ischemia/reperfusion injury by directly targeting BMF and BCL2L13 |
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