Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94
MicroRNA (miR)-150 has been demonstrated to protect the heart from ischemic injury. However, the protective effect of miR‑150 in hypoxia‑injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR‑150 and the underlying molecular mechanisms of miR‑150 in hyp...
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| Veröffentlicht in: | Molecular medicine reports 2018-03, Vol.17 (3), p.4181-4186 |
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| creator | Ma, Jian-Lin Guo, Wen-Ling Chen, Xue-Mei |
| description | MicroRNA (miR)-150 has been demonstrated to protect the heart from ischemic injury. However, the protective effect of miR‑150 in hypoxia‑injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR‑150 and the underlying molecular mechanisms of miR‑150 in hypoxia‑induced cardiomyocyte apoptosis. Using the hypoxia model of human cardiomyocytes (HCMs) in vitro, it was demonstrated that miR‑150 was markedly inhibited in HCMs after hypoxia treatment. Overexpressing miR‑150 significantly decreased hypoxia‑induced HCM death and apoptosis. In addition, GRP94 was revealed to be a direct target of miR‑150. Additionally, GRP94 was demonstrated to be involved in hypoxia‑induced HCM apoptosis, and the protein expression levels of GRP94 were increased in HCMs in the presence of hypoxia. These findings demonstrated that miR‑150 is involved in hypoxia‑mediated gene regulation and apoptosis in HCMs. Furthermore, GRP94 knockout increased the cell viability of hypoxia‑impaired HCMs with miR‑150 mimic or miR‑150 inhibitor transfection. In conclusion, miR‑150 may serve a protective role in cardiomyocyte hypoxia injury, and the underlying mechanism was mediated, at least partially, by inhibiting GRP94 expression. These findings may provide a novel insight for the therapy of hypoxia-induced myocardial I/R injury. |
| doi_str_mv | 10.3892/mmr.2018.8375 |
| format | Article |
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However, the protective effect of miR‑150 in hypoxia‑injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR‑150 and the underlying molecular mechanisms of miR‑150 in hypoxia‑induced cardiomyocyte apoptosis. Using the hypoxia model of human cardiomyocytes (HCMs) in vitro, it was demonstrated that miR‑150 was markedly inhibited in HCMs after hypoxia treatment. Overexpressing miR‑150 significantly decreased hypoxia‑induced HCM death and apoptosis. In addition, GRP94 was revealed to be a direct target of miR‑150. Additionally, GRP94 was demonstrated to be involved in hypoxia‑induced HCM apoptosis, and the protein expression levels of GRP94 were increased in HCMs in the presence of hypoxia. These findings demonstrated that miR‑150 is involved in hypoxia‑mediated gene regulation and apoptosis in HCMs. Furthermore, GRP94 knockout increased the cell viability of hypoxia‑impaired HCMs with miR‑150 mimic or miR‑150 inhibitor transfection. In conclusion, miR‑150 may serve a protective role in cardiomyocyte hypoxia injury, and the underlying mechanism was mediated, at least partially, by inhibiting GRP94 expression. These findings may provide a novel insight for the therapy of hypoxia-induced myocardial I/R injury.</description><identifier>ISSN: 1791-2997</identifier><identifier>EISSN: 1791-3004</identifier><identifier>DOI: 10.3892/mmr.2018.8375</identifier><identifier>PMID: 29328381</identifier><language>eng</language><publisher>Greece: Spandidos Publications</publisher><subject>3' Untranslated Regions ; Anoxia ; Antagomirs - genetics ; Antagomirs - metabolism ; Apoptosis ; Apoptosis - drug effects ; Apoptosis - genetics ; Base Sequence ; Binding Sites ; Biotechnology ; Cardiomyocytes ; Cell Hypoxia ; Cell Line ; Gene expression ; Gene Expression Regulation ; Gene regulation ; Genes, Reporter ; Genetic aspects ; Glucose ; Health aspects ; Heart attacks ; Heart cells ; Humans ; Hypoxia ; Injuries ; Ischemia ; Luciferases - genetics ; Luciferases - metabolism ; Membrane Glycoproteins - genetics ; Membrane Glycoproteins - metabolism ; MicroRNA ; MicroRNAs ; MicroRNAs - agonists ; MicroRNAs - antagonists & inhibitors ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Molecular modelling ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Oligoribonucleotides - genetics ; Oligoribonucleotides - metabolism ; Oxygen - pharmacology ; Proteins ; Rodents ; Signal Transduction ; Transfection</subject><ispartof>Molecular medicine reports, 2018-03, Vol.17 (3), p.4181-4186</ispartof><rights>COPYRIGHT 2018 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2018</rights><rights>Copyright: © Ma et al. 2018</rights><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c482t-6baf852099b4aaef09e628241bea8da6dfb9ae3fd5e7e474a2b4c3c80d5e4c353</citedby><cites>FETCH-LOGICAL-c482t-6baf852099b4aaef09e628241bea8da6dfb9ae3fd5e7e474a2b4c3c80d5e4c353</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,776,780,881,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29328381$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Ma, Jian-Lin</creatorcontrib><creatorcontrib>Guo, Wen-Ling</creatorcontrib><creatorcontrib>Chen, Xue-Mei</creatorcontrib><title>Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94</title><title>Molecular medicine reports</title><addtitle>Mol Med Rep</addtitle><description>MicroRNA (miR)-150 has been demonstrated to protect the heart from ischemic injury. However, the protective effect of miR‑150 in hypoxia‑injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR‑150 and the underlying molecular mechanisms of miR‑150 in hypoxia‑induced cardiomyocyte apoptosis. Using the hypoxia model of human cardiomyocytes (HCMs) in vitro, it was demonstrated that miR‑150 was markedly inhibited in HCMs after hypoxia treatment. Overexpressing miR‑150 significantly decreased hypoxia‑induced HCM death and apoptosis. In addition, GRP94 was revealed to be a direct target of miR‑150. Additionally, GRP94 was demonstrated to be involved in hypoxia‑induced HCM apoptosis, and the protein expression levels of GRP94 were increased in HCMs in the presence of hypoxia. These findings demonstrated that miR‑150 is involved in hypoxia‑mediated gene regulation and apoptosis in HCMs. Furthermore, GRP94 knockout increased the cell viability of hypoxia‑impaired HCMs with miR‑150 mimic or miR‑150 inhibitor transfection. In conclusion, miR‑150 may serve a protective role in cardiomyocyte hypoxia injury, and the underlying mechanism was mediated, at least partially, by inhibiting GRP94 expression. These findings may provide a novel insight for the therapy of hypoxia-induced myocardial I/R injury.</description><subject>3' Untranslated Regions</subject><subject>Anoxia</subject><subject>Antagomirs - genetics</subject><subject>Antagomirs - metabolism</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis - genetics</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Biotechnology</subject><subject>Cardiomyocytes</subject><subject>Cell Hypoxia</subject><subject>Cell Line</subject><subject>Gene expression</subject><subject>Gene Expression Regulation</subject><subject>Gene regulation</subject><subject>Genes, Reporter</subject><subject>Genetic aspects</subject><subject>Glucose</subject><subject>Health aspects</subject><subject>Heart attacks</subject><subject>Heart cells</subject><subject>Humans</subject><subject>Hypoxia</subject><subject>Injuries</subject><subject>Ischemia</subject><subject>Luciferases - genetics</subject><subject>Luciferases - metabolism</subject><subject>Membrane Glycoproteins - genetics</subject><subject>Membrane Glycoproteins - metabolism</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - agonists</subject><subject>MicroRNAs - antagonists & inhibitors</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Molecular modelling</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Oligoribonucleotides - genetics</subject><subject>Oligoribonucleotides - metabolism</subject><subject>Oxygen - pharmacology</subject><subject>Proteins</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Transfection</subject><issn>1791-2997</issn><issn>1791-3004</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptksuLFDEQxoMo7jp69CoBL156zKMfyUUYFl-wuCB6Dul0dU-W7qRN0sv22X_cNDuurkgOKSq_-opKfQi9pGTPhWRvpynsGaFiL3hTPULntJG04ISUj08xk7I5Q89ivCakrlgln6IzJjkTXNBz9PPqBgLczgFitG7AkzXBf_1yKGhFsE4J3KITRHxcZ39rdWFdtxjo8HGZtMNGh876afVmTYANjCPWs5-TjzbidsVJhwHSpjuMi_ERigDDMmbFDs_BJ7CukOVz9KTXY4QXp3uHvn94_-3iU3F59fHzxeGyMKVgqahb3YuKESnbUmvoiYSaCVbSFrTodN31rdTA-66CBsqm1KwtDTeC5EQOKr5D7-5056WdoDPgUtCjmoOddFiV11Y9fHH2qAZ_oypBGBUiC7w5CQT_Y4GY1GTjNrV24JeoqBSyJlzKOqOv_0Gv_RJcHi9Tsmx4XXP6hxr0CMq63ue-ZhNVh4qJsm7qrLdD-_9Q-XSQ1-Ud9DbnHxQUdwV5lzEG6O9npERtrlHZNWpzjdpck_lXf3_MPf3bJvwX8TjAwg</recordid><startdate>20180301</startdate><enddate>20180301</enddate><creator>Ma, Jian-Lin</creator><creator>Guo, Wen-Ling</creator><creator>Chen, Xue-Mei</creator><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><general>D.A. Spandidos</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>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><scope>5PM</scope></search><sort><creationdate>20180301</creationdate><title>Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94</title><author>Ma, Jian-Lin ; Guo, Wen-Ling ; Chen, Xue-Mei</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c482t-6baf852099b4aaef09e628241bea8da6dfb9ae3fd5e7e474a2b4c3c80d5e4c353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>3' Untranslated Regions</topic><topic>Anoxia</topic><topic>Antagomirs - genetics</topic><topic>Antagomirs - metabolism</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis - genetics</topic><topic>Base Sequence</topic><topic>Binding Sites</topic><topic>Biotechnology</topic><topic>Cardiomyocytes</topic><topic>Cell Hypoxia</topic><topic>Cell Line</topic><topic>Gene expression</topic><topic>Gene Expression Regulation</topic><topic>Gene regulation</topic><topic>Genes, Reporter</topic><topic>Genetic aspects</topic><topic>Glucose</topic><topic>Health aspects</topic><topic>Heart attacks</topic><topic>Heart cells</topic><topic>Humans</topic><topic>Hypoxia</topic><topic>Injuries</topic><topic>Ischemia</topic><topic>Luciferases - genetics</topic><topic>Luciferases - metabolism</topic><topic>Membrane Glycoproteins - genetics</topic><topic>Membrane Glycoproteins - metabolism</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - agonists</topic><topic>MicroRNAs - antagonists & inhibitors</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Molecular modelling</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Oligoribonucleotides - genetics</topic><topic>Oligoribonucleotides - metabolism</topic><topic>Oxygen - pharmacology</topic><topic>Proteins</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Transfection</topic><toplevel>online_resources</toplevel><creatorcontrib>Ma, Jian-Lin</creatorcontrib><creatorcontrib>Guo, Wen-Ling</creatorcontrib><creatorcontrib>Chen, Xue-Mei</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>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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Molecular medicine reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Ma, Jian-Lin</au><au>Guo, Wen-Ling</au><au>Chen, Xue-Mei</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94</atitle><jtitle>Molecular medicine reports</jtitle><addtitle>Mol Med Rep</addtitle><date>2018-03-01</date><risdate>2018</risdate><volume>17</volume><issue>3</issue><spage>4181</spage><epage>4186</epage><pages>4181-4186</pages><issn>1791-2997</issn><eissn>1791-3004</eissn><abstract>MicroRNA (miR)-150 has been demonstrated to protect the heart from ischemic injury. However, the protective effect of miR‑150 in hypoxia‑injured cardiomyocytes remains unclear. The present study aimed to investigate the target gene of miR‑150 and the underlying molecular mechanisms of miR‑150 in hypoxia‑induced cardiomyocyte apoptosis. Using the hypoxia model of human cardiomyocytes (HCMs) in vitro, it was demonstrated that miR‑150 was markedly inhibited in HCMs after hypoxia treatment. Overexpressing miR‑150 significantly decreased hypoxia‑induced HCM death and apoptosis. In addition, GRP94 was revealed to be a direct target of miR‑150. Additionally, GRP94 was demonstrated to be involved in hypoxia‑induced HCM apoptosis, and the protein expression levels of GRP94 were increased in HCMs in the presence of hypoxia. These findings demonstrated that miR‑150 is involved in hypoxia‑mediated gene regulation and apoptosis in HCMs. Furthermore, GRP94 knockout increased the cell viability of hypoxia‑impaired HCMs with miR‑150 mimic or miR‑150 inhibitor transfection. In conclusion, miR‑150 may serve a protective role in cardiomyocyte hypoxia injury, and the underlying mechanism was mediated, at least partially, by inhibiting GRP94 expression. These findings may provide a novel insight for the therapy of hypoxia-induced myocardial I/R injury.</abstract><cop>Greece</cop><pub>Spandidos Publications</pub><pmid>29328381</pmid><doi>10.3892/mmr.2018.8375</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | 3' Untranslated Regions Anoxia Antagomirs - genetics Antagomirs - metabolism Apoptosis Apoptosis - drug effects Apoptosis - genetics Base Sequence Binding Sites Biotechnology Cardiomyocytes Cell Hypoxia Cell Line Gene expression Gene Expression Regulation Gene regulation Genes, Reporter Genetic aspects Glucose Health aspects Heart attacks Heart cells Humans Hypoxia Injuries Ischemia Luciferases - genetics Luciferases - metabolism Membrane Glycoproteins - genetics Membrane Glycoproteins - metabolism MicroRNA MicroRNAs MicroRNAs - agonists MicroRNAs - antagonists & inhibitors MicroRNAs - genetics MicroRNAs - metabolism miRNA Molecular modelling Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Oligoribonucleotides - genetics Oligoribonucleotides - metabolism Oxygen - pharmacology Proteins Rodents Signal Transduction Transfection |
| title | Overexpressing microRNA-150 attenuates hypoxia-induced human cardiomyocyte cell apoptosis by targeting glucose-regulated protein-94 |
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