MiR-361-5p promotes oxygen–glucose deprivation/re-oxygenation induced neuronal injury by negatively regulating SQSTM1 in vitro
It has been reported that microRNAs (miRNAs) play essential roles in cerebral ischemia and reperfusion (I/R) injury. This study aimed to explore the role of miR-361-5p in oxygen–glucose deprivation/re-oxygenation-induced neuronal injury in vitro. Cerebral I/R injury cell model was established by usi...
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| Veröffentlicht in: | Metabolic brain disease 2021-12, Vol.36 (8), p.2359-2368 |
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| creator | Zeng, Tao Zhang, Sai He, Yan Liu, Zhenxing Cheng, Qiusheng |
| description | It has been reported that microRNAs (miRNAs) play essential roles in cerebral ischemia and reperfusion (I/R) injury. This study aimed to explore the role of miR-361-5p in oxygen–glucose deprivation/re-oxygenation-induced neuronal injury in vitro. Cerebral I/R injury cell model was established by using PC12 cells exposed to oxygen–glucose deprivation/re-oxygenation (OGD/R). The expression of miR-361-5p and SQSTM1 was evaluated by qRT-PCR or western blot. Neuronal apoptosis was detected by flow cytometry, and cell viability was assessed by CCK-8 assay. The effects of miR-361-5p on the release of LDH and the levels of MDA, SOD, and GSH-Px were investigated by respective detection kits. Dual-luciferase reporter assay and RIP assay were performed to determine the interaction between miR-361-5p and SQSTM1. Rescue experiments were performed to evaluate the function of miR-361-5p and SQSTM1. MiR-361-5p was significantly upregulated, and SQSTM1 was significantly downregulated in OGD/R-stimulated PC12 cells. MiR-361-5p could directly interact with SQSTM1 and negatively regulated it. Inhibition of miR-361-5p efficiently inhibited OGD/R-induced apoptosis and attenuated OGD/R-induced growth defect in PC12 cells. In addition, SQSTM1 overexpression partially attenuates the apoptosis and promoted the viability of OGD/R-treated PC12 cells, which were aggravated by miR-361-5p mimics. Our study demonstrated that miR-361-5p promotes OGD/R-induced neuronal injury via regulating SQSTM1 in PC12 cells. |
| doi_str_mv | 10.1007/s11011-021-00845-x |
| format | Article |
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This study aimed to explore the role of miR-361-5p in oxygen–glucose deprivation/re-oxygenation-induced neuronal injury in vitro. Cerebral I/R injury cell model was established by using PC12 cells exposed to oxygen–glucose deprivation/re-oxygenation (OGD/R). The expression of miR-361-5p and SQSTM1 was evaluated by qRT-PCR or western blot. Neuronal apoptosis was detected by flow cytometry, and cell viability was assessed by CCK-8 assay. The effects of miR-361-5p on the release of LDH and the levels of MDA, SOD, and GSH-Px were investigated by respective detection kits. Dual-luciferase reporter assay and RIP assay were performed to determine the interaction between miR-361-5p and SQSTM1. Rescue experiments were performed to evaluate the function of miR-361-5p and SQSTM1. MiR-361-5p was significantly upregulated, and SQSTM1 was significantly downregulated in OGD/R-stimulated PC12 cells. MiR-361-5p could directly interact with SQSTM1 and negatively regulated it. Inhibition of miR-361-5p efficiently inhibited OGD/R-induced apoptosis and attenuated OGD/R-induced growth defect in PC12 cells. In addition, SQSTM1 overexpression partially attenuates the apoptosis and promoted the viability of OGD/R-treated PC12 cells, which were aggravated by miR-361-5p mimics. Our study demonstrated that miR-361-5p promotes OGD/R-induced neuronal injury via regulating SQSTM1 in PC12 cells.</description><identifier>ISSN: 0885-7490</identifier><identifier>EISSN: 1573-7365</identifier><identifier>DOI: 10.1007/s11011-021-00845-x</identifier><identifier>PMID: 34581931</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Assaying ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cell viability ; Cholecystokinin ; Deprivation ; Evaluation ; Flow cytometry ; Glucose ; Glucose - metabolism ; Injuries ; Ischemia ; Metabolic Diseases ; MicroRNAs - metabolism ; miRNA ; Neurology ; Neurons - metabolism ; Neurosciences ; Oncology ; Original Article ; Oxygen ; Oxygen - metabolism ; Oxygenation ; Pheochromocytoma cells ; Rats ; Reperfusion ; Reperfusion Injury - genetics ; Reperfusion Injury - metabolism ; Sequestosome-1 Protein - genetics ; Sequestosome-1 Protein - metabolism</subject><ispartof>Metabolic brain disease, 2021-12, Vol.36 (8), p.2359-2368</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2021</rights><rights>2021. 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This study aimed to explore the role of miR-361-5p in oxygen–glucose deprivation/re-oxygenation-induced neuronal injury in vitro. Cerebral I/R injury cell model was established by using PC12 cells exposed to oxygen–glucose deprivation/re-oxygenation (OGD/R). The expression of miR-361-5p and SQSTM1 was evaluated by qRT-PCR or western blot. Neuronal apoptosis was detected by flow cytometry, and cell viability was assessed by CCK-8 assay. The effects of miR-361-5p on the release of LDH and the levels of MDA, SOD, and GSH-Px were investigated by respective detection kits. Dual-luciferase reporter assay and RIP assay were performed to determine the interaction between miR-361-5p and SQSTM1. Rescue experiments were performed to evaluate the function of miR-361-5p and SQSTM1. MiR-361-5p was significantly upregulated, and SQSTM1 was significantly downregulated in OGD/R-stimulated PC12 cells. MiR-361-5p could directly interact with SQSTM1 and negatively regulated it. Inhibition of miR-361-5p efficiently inhibited OGD/R-induced apoptosis and attenuated OGD/R-induced growth defect in PC12 cells. In addition, SQSTM1 overexpression partially attenuates the apoptosis and promoted the viability of OGD/R-treated PC12 cells, which were aggravated by miR-361-5p mimics. Our study demonstrated that miR-361-5p promotes OGD/R-induced neuronal injury via regulating SQSTM1 in PC12 cells.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Assaying</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cell viability</subject><subject>Cholecystokinin</subject><subject>Deprivation</subject><subject>Evaluation</subject><subject>Flow cytometry</subject><subject>Glucose</subject><subject>Glucose - metabolism</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Metabolic Diseases</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Neurology</subject><subject>Neurons - metabolism</subject><subject>Neurosciences</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Oxygen</subject><subject>Oxygen - metabolism</subject><subject>Oxygenation</subject><subject>Pheochromocytoma cells</subject><subject>Rats</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - genetics</subject><subject>Reperfusion Injury - metabolism</subject><subject>Sequestosome-1 Protein - genetics</subject><subject>Sequestosome-1 Protein - metabolism</subject><issn>0885-7490</issn><issn>1573-7365</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kc9u1DAQxi1ERZfCC3BAlrhwMfXEsZ0cUVX-SK2q0nK2EmcSZZWNFztebW59B96wT1JvU6jEgYNlzcxvvtHMR8g74J-Ac30aADgA41l6vMgl278gK5BaMC2UfElWvCgk03nJj8nrENaccyGhfEWORS4LKAWsyN1l_4MJBUxu6da7jZswULefOxzv7353Q7QuIG1w6_tdNfVuPPXIlvpjSPuxiRYbOmL0bqyGlFhHP9N6TqkuMTscZuqxi0MKxo7eXN_cXkLC6K6fvHtDjtpqCPj26T8hP7-c3559YxdXX7-ffb5gVmg5sVZxFKBErbC1ZSFkVra6yrBqlK2rXLQ2R6t1IZq6bS3IBpXKCitqKVUGtRAn5OOim7b8FTFMZtMHi8NQjehiMJnUOl1FwQH98A-6dtGn3Q5UmbgygzxR2UJZ70Lw2Jp0o03lZwPcHPwxiz8m-WMe_TH71PT-STrWG2z-tvwxJAFiAUIqjR3659n_kX0Al6aegg</recordid><startdate>20211201</startdate><enddate>20211201</enddate><creator>Zeng, Tao</creator><creator>Zhang, Sai</creator><creator>He, Yan</creator><creator>Liu, Zhenxing</creator><creator>Cheng, Qiusheng</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>7TK</scope><scope>7U7</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88G</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>C1K</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2M</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PSYQQ</scope><scope>Q9U</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-6185-1517</orcidid></search><sort><creationdate>20211201</creationdate><title>MiR-361-5p promotes oxygen–glucose deprivation/re-oxygenation induced neuronal injury by negatively regulating SQSTM1 in vitro</title><author>Zeng, Tao ; Zhang, Sai ; He, Yan ; Liu, Zhenxing ; Cheng, Qiusheng</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-f60e3163b6efc983529f7a2ead6cba43fc4ec7783dbffc15de6628c3b55621b33</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Assaying</topic><topic>Biochemistry</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Cell viability</topic><topic>Cholecystokinin</topic><topic>Deprivation</topic><topic>Evaluation</topic><topic>Flow cytometry</topic><topic>Glucose</topic><topic>Glucose - metabolism</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Metabolic Diseases</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Neurology</topic><topic>Neurons - metabolism</topic><topic>Neurosciences</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Oxygen</topic><topic>Oxygen - metabolism</topic><topic>Oxygenation</topic><topic>Pheochromocytoma cells</topic><topic>Rats</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - genetics</topic><topic>Reperfusion Injury - metabolism</topic><topic>Sequestosome-1 Protein - genetics</topic><topic>Sequestosome-1 Protein - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zeng, Tao</creatorcontrib><creatorcontrib>Zhang, Sai</creatorcontrib><creatorcontrib>He, Yan</creatorcontrib><creatorcontrib>Liu, Zhenxing</creatorcontrib><creatorcontrib>Cheng, Qiusheng</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Neurosciences Abstracts</collection><collection>Toxicology Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Psychology Database (Alumni)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest Psychology</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>ProQuest One Psychology</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><jtitle>Metabolic brain disease</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Zeng, Tao</au><au>Zhang, Sai</au><au>He, Yan</au><au>Liu, Zhenxing</au><au>Cheng, Qiusheng</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MiR-361-5p promotes oxygen–glucose deprivation/re-oxygenation induced neuronal injury by negatively regulating SQSTM1 in vitro</atitle><jtitle>Metabolic brain disease</jtitle><stitle>Metab Brain Dis</stitle><addtitle>Metab Brain Dis</addtitle><date>2021-12-01</date><risdate>2021</risdate><volume>36</volume><issue>8</issue><spage>2359</spage><epage>2368</epage><pages>2359-2368</pages><issn>0885-7490</issn><eissn>1573-7365</eissn><abstract>It has been reported that microRNAs (miRNAs) play essential roles in cerebral ischemia and reperfusion (I/R) injury. This study aimed to explore the role of miR-361-5p in oxygen–glucose deprivation/re-oxygenation-induced neuronal injury in vitro. Cerebral I/R injury cell model was established by using PC12 cells exposed to oxygen–glucose deprivation/re-oxygenation (OGD/R). The expression of miR-361-5p and SQSTM1 was evaluated by qRT-PCR or western blot. Neuronal apoptosis was detected by flow cytometry, and cell viability was assessed by CCK-8 assay. The effects of miR-361-5p on the release of LDH and the levels of MDA, SOD, and GSH-Px were investigated by respective detection kits. Dual-luciferase reporter assay and RIP assay were performed to determine the interaction between miR-361-5p and SQSTM1. Rescue experiments were performed to evaluate the function of miR-361-5p and SQSTM1. MiR-361-5p was significantly upregulated, and SQSTM1 was significantly downregulated in OGD/R-stimulated PC12 cells. MiR-361-5p could directly interact with SQSTM1 and negatively regulated it. Inhibition of miR-361-5p efficiently inhibited OGD/R-induced apoptosis and attenuated OGD/R-induced growth defect in PC12 cells. In addition, SQSTM1 overexpression partially attenuates the apoptosis and promoted the viability of OGD/R-treated PC12 cells, which were aggravated by miR-361-5p mimics. Our study demonstrated that miR-361-5p promotes OGD/R-induced neuronal injury via regulating SQSTM1 in PC12 cells.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>34581931</pmid><doi>10.1007/s11011-021-00845-x</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-6185-1517</orcidid></addata></record> |
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| subjects | Animals Apoptosis Assaying Biochemistry Biomedical and Life Sciences Biomedicine Cell viability Cholecystokinin Deprivation Evaluation Flow cytometry Glucose Glucose - metabolism Injuries Ischemia Metabolic Diseases MicroRNAs - metabolism miRNA Neurology Neurons - metabolism Neurosciences Oncology Original Article Oxygen Oxygen - metabolism Oxygenation Pheochromocytoma cells Rats Reperfusion Reperfusion Injury - genetics Reperfusion Injury - metabolism Sequestosome-1 Protein - genetics Sequestosome-1 Protein - metabolism |
| title | MiR-361-5p promotes oxygen–glucose deprivation/re-oxygenation induced neuronal injury by negatively regulating SQSTM1 in vitro |
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