MiR-19b-3p Inhibits Hypoxia-Ischemia Encephalopathy by Inhibiting SOX6 Expression via Activating Wnt/β-catenin Pathway
Hypoxic-ischemic encephalopathy (HIE) is a detrimental factor in infant death and chronic disease. The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-P...
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| Veröffentlicht in: | Neurochemical research 2023-03, Vol.48 (3), p.874-884 |
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| description | Hypoxic-ischemic encephalopathy (HIE) is a detrimental factor in infant death and chronic disease. The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-PCR assay. HT22 cells were triggered with oxygen-glucose deprivation/reoxygenation (OGD/R) to construct the HIE cell model. Cell Counting Kit-8 (CCK-8) assay was used to estimate viability. SOD and MDA levels were detected by enzyme linked immunosorbent assay. Flow cytometry was implemented to ascertain neurocyte apoptosis. Cellular β-catenin immunofluorescence staining was used to detect the expression and distribution of β-catenin protein. Wnt signaling pathway activation was detected by TOPFlash/FOPFlash luciferase reporter assay. The targeting correlation of SOX6 and miR-19b-3p was corroborated by dual-luciferase reporter gene assay and RNA pull-down assay. MiR-19b-3p expression was once down-regulated, whilst SOX6 expression was up-regulated in HIE patients. MiR-19b-3p overexpression promoted cell proliferation, repressed cell apoptosis, oxidative stress response, and Wnt/β-catenin pathway activation in OGD/R-triggered HT22 cells. MiR-19b-3p negatively regulated SOX6 expression. SOX6 knockdown improved OGD/R-triggered HT22 cells injury via Wnt/β-catenin pathway activation. MiR-19b-3p overexpression suppressed OGD/R-triggered HT22 cell injury via inhibiting SOX6 expression via activating Wnt/β-catenin pathway. |
| doi_str_mv | 10.1007/s11064-022-03812-9 |
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The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-PCR assay. HT22 cells were triggered with oxygen-glucose deprivation/reoxygenation (OGD/R) to construct the HIE cell model. Cell Counting Kit-8 (CCK-8) assay was used to estimate viability. SOD and MDA levels were detected by enzyme linked immunosorbent assay. Flow cytometry was implemented to ascertain neurocyte apoptosis. Cellular β-catenin immunofluorescence staining was used to detect the expression and distribution of β-catenin protein. Wnt signaling pathway activation was detected by TOPFlash/FOPFlash luciferase reporter assay. The targeting correlation of SOX6 and miR-19b-3p was corroborated by dual-luciferase reporter gene assay and RNA pull-down assay. MiR-19b-3p expression was once down-regulated, whilst SOX6 expression was up-regulated in HIE patients. MiR-19b-3p overexpression promoted cell proliferation, repressed cell apoptosis, oxidative stress response, and Wnt/β-catenin pathway activation in OGD/R-triggered HT22 cells. MiR-19b-3p negatively regulated SOX6 expression. SOX6 knockdown improved OGD/R-triggered HT22 cells injury via Wnt/β-catenin pathway activation. MiR-19b-3p overexpression suppressed OGD/R-triggered HT22 cell injury via inhibiting SOX6 expression via activating Wnt/β-catenin pathway.</description><identifier>ISSN: 0364-3190</identifier><identifier>EISSN: 1573-6903</identifier><identifier>DOI: 10.1007/s11064-022-03812-9</identifier><identifier>PMID: 36369428</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Apoptosis ; Apoptosis - genetics ; Assaying ; beta Catenin - metabolism ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Brain damage ; Cell Biology ; Cell injury ; Cell Proliferation ; Cellular stress response ; Cholecystokinin ; Chronic illnesses ; Deprivation ; Encephalopathy ; Enzyme-linked immunosorbent assay ; Flow cytometry ; Gene expression ; Glucose ; Humans ; Hypoxia ; Hypoxia-Ischemia, Brain ; Immunofluorescence ; Infant mortality ; Ischemia ; Kinases ; Luciferases - genetics ; Luciferases - metabolism ; MicroRNAs - genetics ; MicroRNAs - metabolism ; Neurochemistry ; Neurology ; Neurosciences ; Original Paper ; Oxidative stress ; Oxygen ; Pathogenesis ; Reporter gene ; Signal transduction ; SOXD Transcription Factors - metabolism ; Wnt protein ; Wnt Signaling Pathway ; β-Catenin</subject><ispartof>Neurochemical research, 2023-03, Vol.48 (3), p.874-884</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2022. 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The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-PCR assay. HT22 cells were triggered with oxygen-glucose deprivation/reoxygenation (OGD/R) to construct the HIE cell model. Cell Counting Kit-8 (CCK-8) assay was used to estimate viability. SOD and MDA levels were detected by enzyme linked immunosorbent assay. Flow cytometry was implemented to ascertain neurocyte apoptosis. Cellular β-catenin immunofluorescence staining was used to detect the expression and distribution of β-catenin protein. Wnt signaling pathway activation was detected by TOPFlash/FOPFlash luciferase reporter assay. The targeting correlation of SOX6 and miR-19b-3p was corroborated by dual-luciferase reporter gene assay and RNA pull-down assay. MiR-19b-3p expression was once down-regulated, whilst SOX6 expression was up-regulated in HIE patients. MiR-19b-3p overexpression promoted cell proliferation, repressed cell apoptosis, oxidative stress response, and Wnt/β-catenin pathway activation in OGD/R-triggered HT22 cells. MiR-19b-3p negatively regulated SOX6 expression. SOX6 knockdown improved OGD/R-triggered HT22 cells injury via Wnt/β-catenin pathway activation. MiR-19b-3p overexpression suppressed OGD/R-triggered HT22 cell injury via inhibiting SOX6 expression via activating Wnt/β-catenin pathway.</description><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Assaying</subject><subject>beta Catenin - metabolism</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain damage</subject><subject>Cell Biology</subject><subject>Cell injury</subject><subject>Cell Proliferation</subject><subject>Cellular stress response</subject><subject>Cholecystokinin</subject><subject>Chronic illnesses</subject><subject>Deprivation</subject><subject>Encephalopathy</subject><subject>Enzyme-linked immunosorbent assay</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Glucose</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Hypoxia-Ischemia, Brain</subject><subject>Immunofluorescence</subject><subject>Infant mortality</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Luciferases - genetics</subject><subject>Luciferases - metabolism</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>Neurochemistry</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Oxidative stress</subject><subject>Oxygen</subject><subject>Pathogenesis</subject><subject>Reporter gene</subject><subject>Signal transduction</subject><subject>SOXD Transcription Factors - metabolism</subject><subject>Wnt protein</subject><subject>Wnt Signaling Pathway</subject><subject>β-Catenin</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2023</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNp9kc1OGzEYRa2qqITAC3SBRuqmGxfbn8c_S4RSiAQKakGwszyOhxglnul4QpjX6oP0mWoIFIlFV17cc69tHYQ-U_KNEiKPEqVEcEwYwwQUZVh_QCNaSsBCE_iIRgRyDFSTXbSX0j0hucboJ7QLAoTmTI3Q5iL8wFRXGNpiGhehCn0qzoa2eQwWT5Nb-FWwxSQ63y7ssmltvxiKanhlQ7wrfs5uRTF5bDufUmhi8ZALx64PD_Y5von90Z_f2NnexxCLy7ywscM-2qntMvmDl3OMrr9Prk7O8PnsdHpyfI4dyLLHnijFnOIEdMV5NSeOzmvFS89qClI7J0XNSgFWMDVXKv8PwHkQUjpPaQ0wRl-3u23X_Fr71JtVSM4vlzb6Zp0Mk1AqIXjJM_rlHXrfrLuYX5cpWQLwUutMsS3luialztem7cLKdoOhxDxpMVstJmsxz1rMU-nwZXpdrfz8X-XVQwZgC6QcxTvfvd39n9m_LgWXTA</recordid><startdate>20230301</startdate><enddate>20230301</enddate><creator>Zeng, Hao</creator><creator>Chen, Yu-Xia</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>7QR</scope><scope>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>8AO</scope><scope>8FD</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20230301</creationdate><title>MiR-19b-3p Inhibits Hypoxia-Ischemia Encephalopathy by Inhibiting SOX6 Expression via Activating Wnt/β-catenin Pathway</title><author>Zeng, Hao ; Chen, Yu-Xia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-e0882c84039b44bd0c1df845e2f1379cc76f2563a628d8810033ce3677ce11f33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2023</creationdate><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Assaying</topic><topic>beta Catenin - metabolism</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain damage</topic><topic>Cell Biology</topic><topic>Cell injury</topic><topic>Cell Proliferation</topic><topic>Cellular stress response</topic><topic>Cholecystokinin</topic><topic>Chronic illnesses</topic><topic>Deprivation</topic><topic>Encephalopathy</topic><topic>Enzyme-linked immunosorbent assay</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Glucose</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Hypoxia-Ischemia, Brain</topic><topic>Immunofluorescence</topic><topic>Infant mortality</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Luciferases - genetics</topic><topic>Luciferases - metabolism</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>Neurochemistry</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Original Paper</topic><topic>Oxidative stress</topic><topic>Oxygen</topic><topic>Pathogenesis</topic><topic>Reporter gene</topic><topic>Signal transduction</topic><topic>SOXD Transcription Factors - 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Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Hao</au><au>Chen, Yu-Xia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-19b-3p Inhibits Hypoxia-Ischemia Encephalopathy by Inhibiting SOX6 Expression via Activating Wnt/β-catenin Pathway</atitle><jtitle>Neurochemical research</jtitle><stitle>Neurochem Res</stitle><addtitle>Neurochem Res</addtitle><date>2023-03-01</date><risdate>2023</risdate><volume>48</volume><issue>3</issue><spage>874</spage><epage>884</epage><pages>874-884</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><abstract>Hypoxic-ischemic encephalopathy (HIE) is a detrimental factor in infant death and chronic disease. The specific pathogenesis is not entirely clear. Therefore, exploring the pathogenesis of HIE is critical. The expression of miR-19b-3p and SOX6 in umbilical blood of HIE patients was detected by qRT-PCR assay. HT22 cells were triggered with oxygen-glucose deprivation/reoxygenation (OGD/R) to construct the HIE cell model. Cell Counting Kit-8 (CCK-8) assay was used to estimate viability. SOD and MDA levels were detected by enzyme linked immunosorbent assay. Flow cytometry was implemented to ascertain neurocyte apoptosis. Cellular β-catenin immunofluorescence staining was used to detect the expression and distribution of β-catenin protein. Wnt signaling pathway activation was detected by TOPFlash/FOPFlash luciferase reporter assay. The targeting correlation of SOX6 and miR-19b-3p was corroborated by dual-luciferase reporter gene assay and RNA pull-down assay. MiR-19b-3p expression was once down-regulated, whilst SOX6 expression was up-regulated in HIE patients. MiR-19b-3p overexpression promoted cell proliferation, repressed cell apoptosis, oxidative stress response, and Wnt/β-catenin pathway activation in OGD/R-triggered HT22 cells. MiR-19b-3p negatively regulated SOX6 expression. SOX6 knockdown improved OGD/R-triggered HT22 cells injury via Wnt/β-catenin pathway activation. MiR-19b-3p overexpression suppressed OGD/R-triggered HT22 cell injury via inhibiting SOX6 expression via activating Wnt/β-catenin pathway.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>36369428</pmid><doi>10.1007/s11064-022-03812-9</doi><tpages>11</tpages></addata></record> |
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| subjects | Apoptosis Apoptosis - genetics Assaying beta Catenin - metabolism Biochemistry Biomedical and Life Sciences Biomedicine Brain damage Cell Biology Cell injury Cell Proliferation Cellular stress response Cholecystokinin Chronic illnesses Deprivation Encephalopathy Enzyme-linked immunosorbent assay Flow cytometry Gene expression Glucose Humans Hypoxia Hypoxia-Ischemia, Brain Immunofluorescence Infant mortality Ischemia Kinases Luciferases - genetics Luciferases - metabolism MicroRNAs - genetics MicroRNAs - metabolism Neurochemistry Neurology Neurosciences Original Paper Oxidative stress Oxygen Pathogenesis Reporter gene Signal transduction SOXD Transcription Factors - metabolism Wnt protein Wnt Signaling Pathway β-Catenin |
| title | MiR-19b-3p Inhibits Hypoxia-Ischemia Encephalopathy by Inhibiting SOX6 Expression via Activating Wnt/β-catenin Pathway |
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