Long noncoding RNA NEAT1 sponges miR‑125a‑5p to suppress cardiomyocyte apoptosis via BCL2L12
Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. The present study indicated that NEAT1 expression is markedly downreg...
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| Veröffentlicht in: | Molecular medicine reports 2019-05, Vol.19 (5), p.4468-4474 |
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| creator | Yan, Hong Liang, Huasheng Liu, Lie Chen, Dongli Zhang, Qianhuan |
| description | Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. The present study indicated that NEAT1 expression is markedly downregulated in cardiomyocytes following ischemia/reperfusion injury in vivo and hydrogen peroxide treatment in vitro. Further experiments suggested that ectopic overexpression of NEAT1 suppresses cardiomyocyte apoptosis induced by hydrogen peroxide, as assessed by TUNEL assay and flow cytometry. In addition, using a dual‑luciferase reporter assay, NEAT1 was demonstrated to directly interact with microRNA (miR)‑125a‑5p and overexpression of miR‑125a‑5p efficiently reversed the stimulatory effect of NEAT1 on B‑cell lymphoma‑2‑like 12 (BCL2L12) expression. Furthermore, the results indicated that NEAT1 inhibits cardiomyocyte apoptosis via regulating the expression of BCL2L12, which appeared to be mediated via miR‑125a‑5p. In conclusion, the present study suggested that NEAT1 functions as a miR sponge to inhibit cardiomyocyte apoptosis and may be a novel therapeutic target for cardiomyocyte apoptosis‑associated heart diseases. |
| doi_str_mv | 10.3892/mmr.2019.10095 |
| format | Article |
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The present study indicated that NEAT1 expression is markedly downregulated in cardiomyocytes following ischemia/reperfusion injury in vivo and hydrogen peroxide treatment in vitro. Further experiments suggested that ectopic overexpression of NEAT1 suppresses cardiomyocyte apoptosis induced by hydrogen peroxide, as assessed by TUNEL assay and flow cytometry. In addition, using a dual‑luciferase reporter assay, NEAT1 was demonstrated to directly interact with microRNA (miR)‑125a‑5p and overexpression of miR‑125a‑5p efficiently reversed the stimulatory effect of NEAT1 on B‑cell lymphoma‑2‑like 12 (BCL2L12) expression. Furthermore, the results indicated that NEAT1 inhibits cardiomyocyte apoptosis via regulating the expression of BCL2L12, which appeared to be mediated via miR‑125a‑5p. In conclusion, the present study suggested that NEAT1 functions as a miR sponge to inhibit cardiomyocyte apoptosis and may be a novel therapeutic target for cardiomyocyte apoptosis‑associated heart diseases.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2019.10095</identifier><identifier>PMID: 30942442</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>Antisense RNA ; Apoptosis ; B-cell lymphoma ; Binding sites ; Cardiomyocytes ; Cardiovascular disease ; Cardiovascular diseases ; Care and treatment ; Coronary artery disease ; Flow cytometry ; Gene expression ; Genetic aspects ; Heart attacks ; Heart cells ; Heart diseases ; Hydrogen peroxide ; Ischemia ; Journalists ; Kinases ; Luciferase ; Lymphocytes B ; Lymphomas ; Medical research ; MicroRNA ; miRNA ; Myocardial ischemia ; Non-coding RNA ; Novels ; Pathogenesis ; Peroxides ; Proteins ; Reperfusion ; RNA ; Studies ; Therapeutic applications ; Transcription ; Tumors</subject><ispartof>Molecular medicine reports, 2019-05, Vol.19 (5), p.4468-4474</ispartof><rights>COPYRIGHT 2019 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2019</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c430t-9b2580fc0905500f183b0e3f535d77f530f5026e3f750ace3eb6329b7990689e3</citedby><cites>FETCH-LOGICAL-c430t-9b2580fc0905500f183b0e3f535d77f530f5026e3f750ace3eb6329b7990689e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30942442$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Yan, Hong</creatorcontrib><creatorcontrib>Liang, Huasheng</creatorcontrib><creatorcontrib>Liu, Lie</creatorcontrib><creatorcontrib>Chen, Dongli</creatorcontrib><creatorcontrib>Zhang, Qianhuan</creatorcontrib><title>Long noncoding RNA NEAT1 sponges miR‑125a‑5p to suppress cardiomyocyte apoptosis via BCL2L12</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. The present study indicated that NEAT1 expression is markedly downregulated in cardiomyocytes following ischemia/reperfusion injury in vivo and hydrogen peroxide treatment in vitro. Further experiments suggested that ectopic overexpression of NEAT1 suppresses cardiomyocyte apoptosis induced by hydrogen peroxide, as assessed by TUNEL assay and flow cytometry. In addition, using a dual‑luciferase reporter assay, NEAT1 was demonstrated to directly interact with microRNA (miR)‑125a‑5p and overexpression of miR‑125a‑5p efficiently reversed the stimulatory effect of NEAT1 on B‑cell lymphoma‑2‑like 12 (BCL2L12) expression. Furthermore, the results indicated that NEAT1 inhibits cardiomyocyte apoptosis via regulating the expression of BCL2L12, which appeared to be mediated via miR‑125a‑5p. In conclusion, the present study suggested that NEAT1 functions as a miR sponge to inhibit cardiomyocyte apoptosis and may be a novel therapeutic target for cardiomyocyte apoptosis‑associated heart diseases.</description><subject>Antisense RNA</subject><subject>Apoptosis</subject><subject>B-cell lymphoma</subject><subject>Binding sites</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cardiovascular diseases</subject><subject>Care and treatment</subject><subject>Coronary artery disease</subject><subject>Flow cytometry</subject><subject>Gene expression</subject><subject>Genetic aspects</subject><subject>Heart attacks</subject><subject>Heart cells</subject><subject>Heart diseases</subject><subject>Hydrogen peroxide</subject><subject>Ischemia</subject><subject>Journalists</subject><subject>Kinases</subject><subject>Luciferase</subject><subject>Lymphocytes B</subject><subject>Lymphomas</subject><subject>Medical research</subject><subject>MicroRNA</subject><subject>miRNA</subject><subject>Myocardial ischemia</subject><subject>Non-coding RNA</subject><subject>Novels</subject><subject>Pathogenesis</subject><subject>Peroxides</subject><subject>Proteins</subject><subject>Reperfusion</subject><subject>RNA</subject><subject>Studies</subject><subject>Therapeutic applications</subject><subject>Transcription</subject><subject>Tumors</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNptkc9q3DAQxkVJaNKk1x6LIJdcdjMaWbZ13C7pHzAJLJuzIstyUFhbrmQH9pZXyCv2SapNtwmEMIdvmPl9w8BHyBcGc15KvOi6MEdgcs4ApPhAjlkh2YwDZAf7HqUsjsinGO8BcoFCfiRHHGSGWYbH5Lby_R3tfW9841K3ulrQq8vFmtE4pI2NtHOrP49PDIVOIgY6ehqnYQg2Rmp0aJzvtt5sR0v14IfRRxfpg9P027LCiuEpOWz1JtrPez0hN98v18ufs-r6x6_lopqZjMM4kzWKEloDEoQAaFnJa7C8FVw0RZEEWgGYp0khQBvLbZ1zlHUhJeSltPyEnP-7OwT_e7JxVJ2Lxm42urd-igox2fOSYZ7QszfovZ9Cn75LFGNYMibwlbrTG6tc3_oxaLM7qhaiFFlW5pAlav4OlaqxnTO-t61L8_cMJvgYg23VEFynw1YxULtIVYpU7SJVz5Emw9f9t1Pd2eYF_58h_wubBpkm</recordid><startdate>20190501</startdate><enddate>20190501</enddate><creator>Yan, Hong</creator><creator>Liang, Huasheng</creator><creator>Liu, Lie</creator><creator>Chen, Dongli</creator><creator>Zhang, Qianhuan</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20190501</creationdate><title>Long noncoding RNA NEAT1 sponges miR‑125a‑5p to suppress cardiomyocyte apoptosis via BCL2L12</title><author>Yan, Hong ; Liang, Huasheng ; Liu, Lie ; Chen, Dongli ; Zhang, Qianhuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c430t-9b2580fc0905500f183b0e3f535d77f530f5026e3f750ace3eb6329b7990689e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Antisense RNA</topic><topic>Apoptosis</topic><topic>B-cell lymphoma</topic><topic>Binding sites</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Cardiovascular diseases</topic><topic>Care and treatment</topic><topic>Coronary artery disease</topic><topic>Flow cytometry</topic><topic>Gene expression</topic><topic>Genetic aspects</topic><topic>Heart attacks</topic><topic>Heart cells</topic><topic>Heart diseases</topic><topic>Hydrogen peroxide</topic><topic>Ischemia</topic><topic>Journalists</topic><topic>Kinases</topic><topic>Luciferase</topic><topic>Lymphocytes B</topic><topic>Lymphomas</topic><topic>Medical research</topic><topic>MicroRNA</topic><topic>miRNA</topic><topic>Myocardial ischemia</topic><topic>Non-coding RNA</topic><topic>Novels</topic><topic>Pathogenesis</topic><topic>Peroxides</topic><topic>Proteins</topic><topic>Reperfusion</topic><topic>RNA</topic><topic>Studies</topic><topic>Therapeutic applications</topic><topic>Transcription</topic><topic>Tumors</topic><toplevel>online_resources</toplevel><creatorcontrib>Yan, Hong</creatorcontrib><creatorcontrib>Liang, Huasheng</creatorcontrib><creatorcontrib>Liu, Lie</creatorcontrib><creatorcontrib>Chen, Dongli</creatorcontrib><creatorcontrib>Zhang, Qianhuan</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>ProQuest SciTech 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>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>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 Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Biological Science Database</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>MEDLINE - Academic</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Yan, Hong</au><au>Liang, Huasheng</au><au>Liu, Lie</au><au>Chen, Dongli</au><au>Zhang, Qianhuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Long noncoding RNA NEAT1 sponges miR‑125a‑5p to suppress cardiomyocyte apoptosis via BCL2L12</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2019-05-01</date><risdate>2019</risdate><volume>19</volume><issue>5</issue><spage>4468</spage><epage>4474</epage><pages>4468-4474</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>Increasing evidence has suggested that long non‑coding RNA nuclear paraspeckle assembly transcript 1 (NEAT1) has critical roles in multiple biological processes; however, few studies have reported on its function in heart disease. The present study indicated that NEAT1 expression is markedly downregulated in cardiomyocytes following ischemia/reperfusion injury in vivo and hydrogen peroxide treatment in vitro. Further experiments suggested that ectopic overexpression of NEAT1 suppresses cardiomyocyte apoptosis induced by hydrogen peroxide, as assessed by TUNEL assay and flow cytometry. In addition, using a dual‑luciferase reporter assay, NEAT1 was demonstrated to directly interact with microRNA (miR)‑125a‑5p and overexpression of miR‑125a‑5p efficiently reversed the stimulatory effect of NEAT1 on B‑cell lymphoma‑2‑like 12 (BCL2L12) expression. Furthermore, the results indicated that NEAT1 inhibits cardiomyocyte apoptosis via regulating the expression of BCL2L12, which appeared to be mediated via miR‑125a‑5p. In conclusion, the present study suggested that NEAT1 functions as a miR sponge to inhibit cardiomyocyte apoptosis and may be a novel therapeutic target for cardiomyocyte apoptosis‑associated heart diseases.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>30942442</pmid><doi>10.3892/mmr.2019.10095</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Antisense RNA Apoptosis B-cell lymphoma Binding sites Cardiomyocytes Cardiovascular disease Cardiovascular diseases Care and treatment Coronary artery disease Flow cytometry Gene expression Genetic aspects Heart attacks Heart cells Heart diseases Hydrogen peroxide Ischemia Journalists Kinases Luciferase Lymphocytes B Lymphomas Medical research MicroRNA miRNA Myocardial ischemia Non-coding RNA Novels Pathogenesis Peroxides Proteins Reperfusion RNA Studies Therapeutic applications Transcription Tumors |
| title | Long noncoding RNA NEAT1 sponges miR‑125a‑5p to suppress cardiomyocyte apoptosis via BCL2L12 |
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