miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway
Myocardial infarction is the main cause of death in patients with coronary heart disease. At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of ca...
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| description | Myocardial infarction is the main cause of death in patients with coronary heart disease. At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of cardiovascular diseases. It has been reported that mir-451 in microRNA family participates in the protection of myocardial ischemia-reperfusion by regulating AMPK. The aim of this study was to investigate the effect of mir-451 on myocardial ischemia-reperfusion in rats by regulating AMPK signaling pathway. Sixty adult male rats were selected to establish myocardial ischemia-reperfusion animal model by ligating and loosening coronary artery. The expression level of mir-451 was regulated by injection of mir-451 virus vector and antibody, and the effect of increased or decreased mir-451 expression level on the activity of AMPK signaling pathway was detected. The myocardial infarct area and apoptosis rate of myocardial tissue were detected after 75 min ischemia-reperfusion. The results showed that when the expression level of mir-451 decreased by 15.7%, the activity index of AMPK signaling pathway was increased by 18.3%, the infarct area was reduced by 22.4%, and the apoptosis rate of myocardial cells was decreased by 25.2%. At the same time, the pathological structure of myocardial tissue was improved. Therefore, mir-451 is an inhibitor gene of AMPK signaling pathway. Reducing the expression of mir-451 can enhance the activity of AMPK signal pathway, and the increase of AMPK signal pathway activity is beneficial to reduce myocardial ischemia-reperfusion injury. |
| doi_str_mv | 10.1155/2021/9933998 |
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At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of cardiovascular diseases. It has been reported that mir-451 in microRNA family participates in the protection of myocardial ischemia-reperfusion by regulating AMPK. The aim of this study was to investigate the effect of mir-451 on myocardial ischemia-reperfusion in rats by regulating AMPK signaling pathway. Sixty adult male rats were selected to establish myocardial ischemia-reperfusion animal model by ligating and loosening coronary artery. The expression level of mir-451 was regulated by injection of mir-451 virus vector and antibody, and the effect of increased or decreased mir-451 expression level on the activity of AMPK signaling pathway was detected. The myocardial infarct area and apoptosis rate of myocardial tissue were detected after 75 min ischemia-reperfusion. The results showed that when the expression level of mir-451 decreased by 15.7%, the activity index of AMPK signaling pathway was increased by 18.3%, the infarct area was reduced by 22.4%, and the apoptosis rate of myocardial cells was decreased by 25.2%. At the same time, the pathological structure of myocardial tissue was improved. Therefore, mir-451 is an inhibitor gene of AMPK signaling pathway. Reducing the expression of mir-451 can enhance the activity of AMPK signal pathway, and the increase of AMPK signal pathway activity is beneficial to reduce myocardial ischemia-reperfusion injury.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2021/9933998</identifier><identifier>PMID: 34307674</identifier><language>eng</language><publisher>LONDON: Hindawi</publisher><subject>Adenylic acid ; AMP-Activated Protein Kinases - metabolism ; Analysis ; Animal models ; Animals ; Antibodies ; Antioxidants ; Apoptosis ; Apoptosis - genetics ; Biotechnology & Applied Microbiology ; Cardiac arrhythmia ; Cardiomyocytes ; Cardiovascular diseases ; Care and treatment ; Coronary artery ; Coronary artery disease ; Cytokines ; Diagnosis ; Down-Regulation - genetics ; Enzymes ; Free radicals ; Gene expression ; Gene therapy ; Genes ; Genetic aspects ; Health aspects ; Heart attack ; Heart attacks ; Heart diseases ; Identification and classification ; Inflammation - pathology ; Injury prevention ; Ischemia ; Kinases ; Life Sciences & Biomedicine ; Medicine, Research & Experimental ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; MicroRNAs - metabolism ; miRNA ; Myocardial infarction ; Myocardial Infarction - genetics ; Myocardial ischemia ; Myocardial Reperfusion Injury - enzymology ; Myocardial Reperfusion Injury - genetics ; Nanoparticles ; Oxidative stress ; Patient outcomes ; Perfusion ; Physiological aspects ; Physiology ; Prevention ; Properties ; Protein kinases ; Rats ; Reperfusion ; Research & Experimental Medicine ; Ribonucleic acid ; Risk factors ; RNA ; Science & Technology ; Signal Transduction ; Signaling ; Viruses</subject><ispartof>BioMed research international, 2021, Vol.2021, p.9933998-9, Article 9933998</ispartof><rights>Copyright © 2021 Yulin Guo et al.</rights><rights>COPYRIGHT 2021 John Wiley & Sons, Inc.</rights><rights>Copyright © 2021 Yulin Guo et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2021 Yulin Guo et al. 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>6</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000675805600002</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c504t-df2dc1124ff4b194273f9a874935f751dc72d138b1a6a7d27723112c0584bb7e3</citedby><cites>FETCH-LOGICAL-c504t-df2dc1124ff4b194273f9a874935f751dc72d138b1a6a7d27723112c0584bb7e3</cites><orcidid>0000-0001-9024-6597</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8279856/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8279856/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,4025,27928,27929,27930,39263,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34307674$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Liu, Junyan</contributor><contributor>Junyan Liu</contributor><creatorcontrib>Guo, Yulin</creatorcontrib><creatorcontrib>Gao, Jie</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><creatorcontrib>Zhang, Xitao</creatorcontrib><creatorcontrib>An, Xiangguang</creatorcontrib><creatorcontrib>Zhou, Jian</creatorcontrib><creatorcontrib>Su, Pixiong</creatorcontrib><title>miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway</title><title>BioMed research international</title><addtitle>BIOMED RES INT</addtitle><addtitle>Biomed Res Int</addtitle><description>Myocardial infarction is the main cause of death in patients with coronary heart disease. At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of cardiovascular diseases. It has been reported that mir-451 in microRNA family participates in the protection of myocardial ischemia-reperfusion by regulating AMPK. The aim of this study was to investigate the effect of mir-451 on myocardial ischemia-reperfusion in rats by regulating AMPK signaling pathway. Sixty adult male rats were selected to establish myocardial ischemia-reperfusion animal model by ligating and loosening coronary artery. The expression level of mir-451 was regulated by injection of mir-451 virus vector and antibody, and the effect of increased or decreased mir-451 expression level on the activity of AMPK signaling pathway was detected. The myocardial infarct area and apoptosis rate of myocardial tissue were detected after 75 min ischemia-reperfusion. The results showed that when the expression level of mir-451 decreased by 15.7%, the activity index of AMPK signaling pathway was increased by 18.3%, the infarct area was reduced by 22.4%, and the apoptosis rate of myocardial cells was decreased by 25.2%. At the same time, the pathological structure of myocardial tissue was improved. Therefore, mir-451 is an inhibitor gene of AMPK signaling pathway. Reducing the expression of mir-451 can enhance the activity of AMPK signal pathway, and the increase of AMPK signal pathway activity is beneficial to reduce myocardial ischemia-reperfusion injury.</description><subject>Adenylic acid</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Analysis</subject><subject>Animal models</subject><subject>Animals</subject><subject>Antibodies</subject><subject>Antioxidants</subject><subject>Apoptosis</subject><subject>Apoptosis - genetics</subject><subject>Biotechnology & Applied Microbiology</subject><subject>Cardiac arrhythmia</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular diseases</subject><subject>Care and treatment</subject><subject>Coronary artery</subject><subject>Coronary artery disease</subject><subject>Cytokines</subject><subject>Diagnosis</subject><subject>Down-Regulation - genetics</subject><subject>Enzymes</subject><subject>Free radicals</subject><subject>Gene expression</subject><subject>Gene therapy</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Health aspects</subject><subject>Heart attack</subject><subject>Heart attacks</subject><subject>Heart diseases</subject><subject>Identification and classification</subject><subject>Inflammation - pathology</subject><subject>Injury prevention</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Life Sciences & Biomedicine</subject><subject>Medicine, Research & Experimental</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>MicroRNAs - metabolism</subject><subject>miRNA</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - genetics</subject><subject>Myocardial ischemia</subject><subject>Myocardial Reperfusion Injury - enzymology</subject><subject>Myocardial Reperfusion Injury - genetics</subject><subject>Nanoparticles</subject><subject>Oxidative stress</subject><subject>Patient outcomes</subject><subject>Perfusion</subject><subject>Physiological aspects</subject><subject>Physiology</subject><subject>Prevention</subject><subject>Properties</subject><subject>Protein kinases</subject><subject>Rats</subject><subject>Reperfusion</subject><subject>Research & Experimental Medicine</subject><subject>Ribonucleic acid</subject><subject>Risk factors</subject><subject>RNA</subject><subject>Science & Technology</subject><subject>Signal Transduction</subject><subject>Signaling</subject><subject>Viruses</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>HGBXW</sourceid><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>eNqNkstv1DAQxiMEolXpjTOKxAUJQv1-XJBWKx4VragWEEfLceysq8Re4oTV_vc47LIFDhW-2Nb85vOM5yuKpxC8hpDSCwQQvJASYynFg-IUYUgqBgl8eDxjfFKcp3QL8hKQAckeFyeYYMAZJ6fFt96vKkJhGUN5vYtGD43XXXmZzNr2Xlcru7GDm5LPcR_KlR5TWe_KlW2nTo8-tOXi-uZj-dm3QXfz9UaP663ePSkeOd0le37Yz4qv795-WX6orj69v1wuripDARmrxqHGQIiIc6SGkiCOndSCE4mp4xQ2hqMGYlFDzTRvEOe5LYgMoILUNbf4rHiz191MdW8bY8M46E5tBt_rYaei9urvSPBr1cYfSiAuBWVZ4MVBYIjfJ5tG1ftkbNfpYOOUFKKUYoIooBl9_g96G6ch9_2LQpwwgcQd1erOKh9czO-aWVQtmGRCcCro_ZTAlEvJcaZe7SkzxJQG646NQaBmA6jZAOpggIw_-_MzjvDvcWdA7IGtraNLxttg7BHLDmG5OEDZbBa09GOecAzLOIUxp778_9Q7eu1Do7f-_rp_AgkP1F8</recordid><startdate>2021</startdate><enddate>2021</enddate><creator>Guo, Yulin</creator><creator>Gao, Jie</creator><creator>Liu, Yan</creator><creator>Zhang, Xitao</creator><creator>An, Xiangguang</creator><creator>Zhou, Jian</creator><creator>Su, Pixiong</creator><general>Hindawi</general><general>Hindawi Publishing Group</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>RHU</scope><scope>RHW</scope><scope>RHX</scope><scope>BLEPL</scope><scope>DTL</scope><scope>HGBXW</scope><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>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</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>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0001-9024-6597</orcidid></search><sort><creationdate>2021</creationdate><title>miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway</title><author>Guo, Yulin ; Gao, Jie ; Liu, Yan ; Zhang, Xitao ; An, Xiangguang ; Zhou, Jian ; Su, Pixiong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c504t-df2dc1124ff4b194273f9a874935f751dc72d138b1a6a7d27723112c0584bb7e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>Adenylic acid</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Analysis</topic><topic>Animal models</topic><topic>Animals</topic><topic>Antibodies</topic><topic>Antioxidants</topic><topic>Apoptosis</topic><topic>Apoptosis - genetics</topic><topic>Biotechnology & Applied Microbiology</topic><topic>Cardiac arrhythmia</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular diseases</topic><topic>Care and treatment</topic><topic>Coronary artery</topic><topic>Coronary artery disease</topic><topic>Cytokines</topic><topic>Diagnosis</topic><topic>Down-Regulation - genetics</topic><topic>Enzymes</topic><topic>Free radicals</topic><topic>Gene expression</topic><topic>Gene therapy</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Health aspects</topic><topic>Heart attack</topic><topic>Heart attacks</topic><topic>Heart diseases</topic><topic>Identification and classification</topic><topic>Inflammation - pathology</topic><topic>Injury prevention</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Life Sciences & Biomedicine</topic><topic>Medicine, Research & Experimental</topic><topic>MicroRNA</topic><topic>MicroRNAs</topic><topic>MicroRNAs - genetics</topic><topic>MicroRNAs - metabolism</topic><topic>miRNA</topic><topic>Myocardial infarction</topic><topic>Myocardial Infarction - genetics</topic><topic>Myocardial ischemia</topic><topic>Myocardial Reperfusion Injury - enzymology</topic><topic>Myocardial Reperfusion Injury - genetics</topic><topic>Nanoparticles</topic><topic>Oxidative stress</topic><topic>Patient outcomes</topic><topic>Perfusion</topic><topic>Physiological aspects</topic><topic>Physiology</topic><topic>Prevention</topic><topic>Properties</topic><topic>Protein kinases</topic><topic>Rats</topic><topic>Reperfusion</topic><topic>Research & Experimental Medicine</topic><topic>Ribonucleic acid</topic><topic>Risk factors</topic><topic>RNA</topic><topic>Science & Technology</topic><topic>Signal Transduction</topic><topic>Signaling</topic><topic>Viruses</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Guo, Yulin</creatorcontrib><creatorcontrib>Gao, Jie</creatorcontrib><creatorcontrib>Liu, Yan</creatorcontrib><creatorcontrib>Zhang, Xitao</creatorcontrib><creatorcontrib>An, Xiangguang</creatorcontrib><creatorcontrib>Zhou, Jian</creatorcontrib><creatorcontrib>Su, Pixiong</creatorcontrib><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Guo, Yulin</au><au>Gao, Jie</au><au>Liu, Yan</au><au>Zhang, Xitao</au><au>An, Xiangguang</au><au>Zhou, Jian</au><au>Su, Pixiong</au><au>Liu, Junyan</au><au>Junyan Liu</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway</atitle><jtitle>BioMed research international</jtitle><stitle>BIOMED RES INT</stitle><addtitle>Biomed Res Int</addtitle><date>2021</date><risdate>2021</risdate><volume>2021</volume><spage>9933998</spage><epage>9</epage><pages>9933998-9</pages><artnum>9933998</artnum><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Myocardial infarction is the main cause of death in patients with coronary heart disease. At present, the main method to treat cardiovascular disease is perfusion therapy. Myocardial ischemia-reperfusion will inevitably lead to reperfusion injury, which is also a major problem in the treatment of cardiovascular diseases. It has been reported that mir-451 in microRNA family participates in the protection of myocardial ischemia-reperfusion by regulating AMPK. The aim of this study was to investigate the effect of mir-451 on myocardial ischemia-reperfusion in rats by regulating AMPK signaling pathway. Sixty adult male rats were selected to establish myocardial ischemia-reperfusion animal model by ligating and loosening coronary artery. The expression level of mir-451 was regulated by injection of mir-451 virus vector and antibody, and the effect of increased or decreased mir-451 expression level on the activity of AMPK signaling pathway was detected. The myocardial infarct area and apoptosis rate of myocardial tissue were detected after 75 min ischemia-reperfusion. The results showed that when the expression level of mir-451 decreased by 15.7%, the activity index of AMPK signaling pathway was increased by 18.3%, the infarct area was reduced by 22.4%, and the apoptosis rate of myocardial cells was decreased by 25.2%. At the same time, the pathological structure of myocardial tissue was improved. Therefore, mir-451 is an inhibitor gene of AMPK signaling pathway. Reducing the expression of mir-451 can enhance the activity of AMPK signal pathway, and the increase of AMPK signal pathway activity is beneficial to reduce myocardial ischemia-reperfusion injury.</abstract><cop>LONDON</cop><pub>Hindawi</pub><pmid>34307674</pmid><doi>10.1155/2021/9933998</doi><tpages>9</tpages><orcidid>https://orcid.org/0000-0001-9024-6597</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Adenylic acid AMP-Activated Protein Kinases - metabolism Analysis Animal models Animals Antibodies Antioxidants Apoptosis Apoptosis - genetics Biotechnology & Applied Microbiology Cardiac arrhythmia Cardiomyocytes Cardiovascular diseases Care and treatment Coronary artery Coronary artery disease Cytokines Diagnosis Down-Regulation - genetics Enzymes Free radicals Gene expression Gene therapy Genes Genetic aspects Health aspects Heart attack Heart attacks Heart diseases Identification and classification Inflammation - pathology Injury prevention Ischemia Kinases Life Sciences & Biomedicine Medicine, Research & Experimental MicroRNA MicroRNAs MicroRNAs - genetics MicroRNAs - metabolism miRNA Myocardial infarction Myocardial Infarction - genetics Myocardial ischemia Myocardial Reperfusion Injury - enzymology Myocardial Reperfusion Injury - genetics Nanoparticles Oxidative stress Patient outcomes Perfusion Physiological aspects Physiology Prevention Properties Protein kinases Rats Reperfusion Research & Experimental Medicine Ribonucleic acid Risk factors RNA Science & Technology Signal Transduction Signaling Viruses |
| title | miR-451 on Myocardial Ischemia-Reperfusion in Rats by Regulating AMPK Signaling Pathway |
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