MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network
Oxidative stress plays an important role in cardiovascular diseases. Studies have shown that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which can be the result of oxidative stress. This study was designed to determine whether increased miR-1 levels lead to alteration...
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| Veröffentlicht in: | Cell stress & chaperones 2015-05, Vol.20 (3), p.411-420 |
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| creator | Wang, Lu Yuan, Ye Li, Jing Ren, Hequn Cai, Qingxin Chen, Xu Liang, Haihai Shan, Hongli Fu, Zidong Donna Gao, Xu Lv, Yanjie Yang, Baofeng Zhang, Yan |
| description | Oxidative stress plays an important role in cardiovascular diseases. Studies have shown that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which can be the result of oxidative stress. This study was designed to determine whether increased miR-1 levels lead to alterations in the expression of proteins related to oxidative stress, which could contribute to heart dysfunction. We compared cardiac function in wild-type (WT) and miR-1 transgene (miR-1/Tg) C57BL/6 mice (n≥10/group). Echocardiography showed that stroke volume (SV), ejection fraction (EF), and fractional shortening (FS) were significantly decreased in miR-1/Tg mice. Concomitantly, the level of reactive oxygen species (ROS) was elevated in the cardiomyocytes from the miR-1/Tg mice, and activities of lactate dehydrogenase (LDH) and creatinine kinase (CK) in plasma were also increased in the miR-1/Tg mice. All of these changes could be reversed by LNA-anti-miR-1. In the cardiomyocytes of neonatal Wistar rats, overexpression of miR-1 exhibits higher ROS levels and lower resistance to H2O2-induced oxidative stress. We demonstrated that SOD1, Gclc, and G6PD are novel targets of miR-1 for post-transcriptional repression. MicroRNA-1 post-transcriptionally represses the expression of SOD1, Gclc, and G6PD, which is likely to contribute to the increased ROS level and the susceptibility to oxidative stress of the hearts of miR-1 transgenic mice. |
| doi_str_mv | 10.1007/s12192-014-0565-9 |
| format | Article |
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Studies have shown that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which can be the result of oxidative stress. This study was designed to determine whether increased miR-1 levels lead to alterations in the expression of proteins related to oxidative stress, which could contribute to heart dysfunction. We compared cardiac function in wild-type (WT) and miR-1 transgene (miR-1/Tg) C57BL/6 mice (n≥10/group). Echocardiography showed that stroke volume (SV), ejection fraction (EF), and fractional shortening (FS) were significantly decreased in miR-1/Tg mice. Concomitantly, the level of reactive oxygen species (ROS) was elevated in the cardiomyocytes from the miR-1/Tg mice, and activities of lactate dehydrogenase (LDH) and creatinine kinase (CK) in plasma were also increased in the miR-1/Tg mice. All of these changes could be reversed by LNA-anti-miR-1. In the cardiomyocytes of neonatal Wistar rats, overexpression of miR-1 exhibits higher ROS levels and lower resistance to H2O2-induced oxidative stress. We demonstrated that SOD1, Gclc, and G6PD are novel targets of miR-1 for post-transcriptional repression. MicroRNA-1 post-transcriptionally represses the expression of SOD1, Gclc, and G6PD, which is likely to contribute to the increased ROS level and the susceptibility to oxidative stress of the hearts of miR-1 transgenic mice.</description><identifier>ISSN: 1355-8145</identifier><identifier>EISSN: 1466-1268</identifier><identifier>DOI: 10.1007/s12192-014-0565-9</identifier><identifier>PMID: 25583113</identifier><language>eng</language><publisher>Dordrecht: Springer</publisher><subject>Animals ; Antioxidants - metabolism ; Apoptosis ; Base Sequence ; Binding Sites ; Biochemistry ; Biomedical and Life Sciences ; Biomedicine ; Cancer Research ; Cell Biology ; Cells, Cultured ; Enzyme Repression ; Enzymes ; Glucosephosphate Dehydrogenase - genetics ; Glucosephosphate Dehydrogenase - metabolism ; Glutamate-Cysteine Ligase - genetics ; Glutamate-Cysteine Ligase - metabolism ; Heart ; Immunology ; Male ; Messenger RNA ; Mice, Inbred C57BL ; Mice, Transgenic ; MicroRNA ; MicroRNAs - genetics ; Myocardium ; Myocytes, Cardiac - enzymology ; Neurosciences ; Original Paper ; Oxidative Stress ; Promoter Regions, Genetic ; Rats, Wistar ; Reactive oxygen species ; Reactive Oxygen Species - metabolism ; RNA Interference ; Superoxide Dismutase - genetics ; Superoxide Dismutase - metabolism ; Superoxide Dismutase-1 ; Three prime untranslated regions ; Transgenic animals</subject><ispartof>Cell stress & chaperones, 2015-05, Vol.20 (3), p.411-420</ispartof><rights>Cell Stress Society International 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c562t-ed875861eb4efa1839876159ebb8e5be9f2e31d8536d43e3e49aad905126d7623</citedby><cites>FETCH-LOGICAL-c562t-ed875861eb4efa1839876159ebb8e5be9f2e31d8536d43e3e49aad905126d7623</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.jstor.org/stable/pdf/24671582$$EPDF$$P50$$Gjstor$$H</linktopdf><linktohtml>$$Uhttps://www.jstor.org/stable/24671582$$EHTML$$P50$$Gjstor$$H</linktohtml><link.rule.ids>230,314,727,780,784,803,885,27924,27925,41488,42557,51319,53791,53793,58017,58250</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/25583113$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wang, Lu</creatorcontrib><creatorcontrib>Yuan, Ye</creatorcontrib><creatorcontrib>Li, Jing</creatorcontrib><creatorcontrib>Ren, Hequn</creatorcontrib><creatorcontrib>Cai, Qingxin</creatorcontrib><creatorcontrib>Chen, Xu</creatorcontrib><creatorcontrib>Liang, Haihai</creatorcontrib><creatorcontrib>Shan, Hongli</creatorcontrib><creatorcontrib>Fu, Zidong Donna</creatorcontrib><creatorcontrib>Gao, Xu</creatorcontrib><creatorcontrib>Lv, Yanjie</creatorcontrib><creatorcontrib>Yang, Baofeng</creatorcontrib><creatorcontrib>Zhang, Yan</creatorcontrib><title>MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network</title><title>Cell stress & chaperones</title><addtitle>Cell Stress and Chaperones</addtitle><addtitle>Cell Stress Chaperones</addtitle><description>Oxidative stress plays an important role in cardiovascular diseases. Studies have shown that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which can be the result of oxidative stress. This study was designed to determine whether increased miR-1 levels lead to alterations in the expression of proteins related to oxidative stress, which could contribute to heart dysfunction. We compared cardiac function in wild-type (WT) and miR-1 transgene (miR-1/Tg) C57BL/6 mice (n≥10/group). Echocardiography showed that stroke volume (SV), ejection fraction (EF), and fractional shortening (FS) were significantly decreased in miR-1/Tg mice. Concomitantly, the level of reactive oxygen species (ROS) was elevated in the cardiomyocytes from the miR-1/Tg mice, and activities of lactate dehydrogenase (LDH) and creatinine kinase (CK) in plasma were also increased in the miR-1/Tg mice. All of these changes could be reversed by LNA-anti-miR-1. In the cardiomyocytes of neonatal Wistar rats, overexpression of miR-1 exhibits higher ROS levels and lower resistance to H2O2-induced oxidative stress. We demonstrated that SOD1, Gclc, and G6PD are novel targets of miR-1 for post-transcriptional repression. MicroRNA-1 post-transcriptionally represses the expression of SOD1, Gclc, and G6PD, which is likely to contribute to the increased ROS level and the susceptibility to oxidative stress of the hearts of miR-1 transgenic mice.</description><subject>Animals</subject><subject>Antioxidants - metabolism</subject><subject>Apoptosis</subject><subject>Base Sequence</subject><subject>Binding Sites</subject><subject>Biochemistry</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Cancer Research</subject><subject>Cell Biology</subject><subject>Cells, Cultured</subject><subject>Enzyme Repression</subject><subject>Enzymes</subject><subject>Glucosephosphate Dehydrogenase - genetics</subject><subject>Glucosephosphate Dehydrogenase - metabolism</subject><subject>Glutamate-Cysteine Ligase - genetics</subject><subject>Glutamate-Cysteine Ligase - metabolism</subject><subject>Heart</subject><subject>Immunology</subject><subject>Male</subject><subject>Messenger RNA</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Transgenic</subject><subject>MicroRNA</subject><subject>MicroRNAs - genetics</subject><subject>Myocardium</subject><subject>Myocytes, Cardiac - enzymology</subject><subject>Neurosciences</subject><subject>Original Paper</subject><subject>Oxidative Stress</subject><subject>Promoter Regions, Genetic</subject><subject>Rats, Wistar</subject><subject>Reactive oxygen species</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>RNA Interference</subject><subject>Superoxide Dismutase - genetics</subject><subject>Superoxide Dismutase - metabolism</subject><subject>Superoxide Dismutase-1</subject><subject>Three prime untranslated regions</subject><subject>Transgenic animals</subject><issn>1355-8145</issn><issn>1466-1268</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</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>eNp9UctuFDEQHCEQCYEP4ACylAsXg9uv8VyQooiXFEBCcLY8Mz0bL7v2YnsX8vd4mBACB052q6uqq7ua5jGw58BY-yIDh45TBpIypRXt7jTHILWmwLW5W_9CKWpAqqPmQc5rVjltC_ebI66UEQDiuAnv_ZDipw9nFIhbrZI7uIKZDC6N3g0k_vCjK_6AJJeEOZP-iuxiLrQkF_KQ_K74GNyGbOPoJz-4uSRxIuUSiQu1mgVCIQHL95i-PmzuTW6T8dH1e9J8ef3q8_lbevHxzbvzsws6KM0LxdG0ymjAXuLkwIjOtBpUh31vUPXYTRwFjEYJPUqBAmXn3NgxVRcfW83FSfNy0d3t-y2OA4ZqeGN3yW9durLReft3J_hLu4oHKyXTnWBV4Nm1QIrf9piL3fo84GbjAsZ9tqCrwVaadp51-g90HfepHuUXSnbADJ9RsKDquXNOON2YAWbnNO2Spq1p2jlN21XO09tb3DB-x1cBfAHk2gorTLdG_0f1yUJa5xLTH1GpW1CGi5_ab7Zg</recordid><startdate>20150501</startdate><enddate>20150501</enddate><creator>Wang, Lu</creator><creator>Yuan, Ye</creator><creator>Li, Jing</creator><creator>Ren, Hequn</creator><creator>Cai, Qingxin</creator><creator>Chen, Xu</creator><creator>Liang, Haihai</creator><creator>Shan, Hongli</creator><creator>Fu, Zidong Donna</creator><creator>Gao, Xu</creator><creator>Lv, Yanjie</creator><creator>Yang, Baofeng</creator><creator>Zhang, Yan</creator><general>Springer</general><general>Springer Netherlands</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>7QL</scope><scope>7QP</scope><scope>7T7</scope><scope>7TK</scope><scope>7TM</scope><scope>7U9</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>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P64</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20150501</creationdate><title>MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network</title><author>Wang, Lu ; Yuan, Ye ; Li, Jing ; Ren, Hequn ; Cai, Qingxin ; Chen, Xu ; Liang, Haihai ; Shan, Hongli ; Fu, Zidong Donna ; Gao, Xu ; Lv, Yanjie ; Yang, Baofeng ; Zhang, Yan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c562t-ed875861eb4efa1839876159ebb8e5be9f2e31d8536d43e3e49aad905126d7623</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Animals</topic><topic>Antioxidants - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Cell stress & chaperones</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Lu</au><au>Yuan, Ye</au><au>Li, Jing</au><au>Ren, Hequn</au><au>Cai, Qingxin</au><au>Chen, Xu</au><au>Liang, Haihai</au><au>Shan, Hongli</au><au>Fu, Zidong Donna</au><au>Gao, Xu</au><au>Lv, Yanjie</au><au>Yang, Baofeng</au><au>Zhang, Yan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network</atitle><jtitle>Cell stress & chaperones</jtitle><stitle>Cell Stress and Chaperones</stitle><addtitle>Cell Stress Chaperones</addtitle><date>2015-05-01</date><risdate>2015</risdate><volume>20</volume><issue>3</issue><spage>411</spage><epage>420</epage><pages>411-420</pages><issn>1355-8145</issn><eissn>1466-1268</eissn><abstract>Oxidative stress plays an important role in cardiovascular diseases. Studies have shown that miR-1 plays an important role in the regulation of cardiomyocyte apoptosis, which can be the result of oxidative stress. This study was designed to determine whether increased miR-1 levels lead to alterations in the expression of proteins related to oxidative stress, which could contribute to heart dysfunction. We compared cardiac function in wild-type (WT) and miR-1 transgene (miR-1/Tg) C57BL/6 mice (n≥10/group). Echocardiography showed that stroke volume (SV), ejection fraction (EF), and fractional shortening (FS) were significantly decreased in miR-1/Tg mice. Concomitantly, the level of reactive oxygen species (ROS) was elevated in the cardiomyocytes from the miR-1/Tg mice, and activities of lactate dehydrogenase (LDH) and creatinine kinase (CK) in plasma were also increased in the miR-1/Tg mice. All of these changes could be reversed by LNA-anti-miR-1. In the cardiomyocytes of neonatal Wistar rats, overexpression of miR-1 exhibits higher ROS levels and lower resistance to H2O2-induced oxidative stress. We demonstrated that SOD1, Gclc, and G6PD are novel targets of miR-1 for post-transcriptional repression. MicroRNA-1 post-transcriptionally represses the expression of SOD1, Gclc, and G6PD, which is likely to contribute to the increased ROS level and the susceptibility to oxidative stress of the hearts of miR-1 transgenic mice.</abstract><cop>Dordrecht</cop><pub>Springer</pub><pmid>25583113</pmid><doi>10.1007/s12192-014-0565-9</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Cell stress & chaperones, 2015-05, Vol.20 (3), p.411-420 |
| issn | 1355-8145 1466-1268 |
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| subjects | Animals Antioxidants - metabolism Apoptosis Base Sequence Binding Sites Biochemistry Biomedical and Life Sciences Biomedicine Cancer Research Cell Biology Cells, Cultured Enzyme Repression Enzymes Glucosephosphate Dehydrogenase - genetics Glucosephosphate Dehydrogenase - metabolism Glutamate-Cysteine Ligase - genetics Glutamate-Cysteine Ligase - metabolism Heart Immunology Male Messenger RNA Mice, Inbred C57BL Mice, Transgenic MicroRNA MicroRNAs - genetics Myocardium Myocytes, Cardiac - enzymology Neurosciences Original Paper Oxidative Stress Promoter Regions, Genetic Rats, Wistar Reactive oxygen species Reactive Oxygen Species - metabolism RNA Interference Superoxide Dismutase - genetics Superoxide Dismutase - metabolism Superoxide Dismutase-1 Three prime untranslated regions Transgenic animals |
| title | MicroRNA-1 aggravates cardiac oxidative stress by post-transcriptional modification of the antioxidant network |
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