Adiponectin Upregulates MiR-133a in Cardiac Hypertrophy through AMPK Activation and Reduced ERK1/2 Phosphorylation
Adiponectin and miR-133a are key regulators in cardiac hypertrophy. However, whether APN has a potential effect on miR-133a remains unclear. In this study, we aimed to investigate whether APN could regulate miR-133a expression in Angiotensin II (Ang II) induced cardiac hypertrophy in vivo and in vit...
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| creator | Li, Ying Cai, Xiaojun Guan, Yuqing Wang, Lei Wang, Shuya Li, Yueyan Fu, Ying Gao, Xiaoyuan Su, Guohai |
| description | Adiponectin and miR-133a are key regulators in cardiac hypertrophy. However, whether APN has a potential effect on miR-133a remains unclear. In this study, we aimed to investigate whether APN could regulate miR-133a expression in Angiotensin II (Ang II) induced cardiac hypertrophy in vivo and in vitro. Lentiviral-mediated adiponectin treatment attenuated cardiac hypertrophy induced by Ang II infusion in male wistar rats as determined by reduced cell surface area and mRNA levels of atrial natriuretic peptide (ANF) and brain natriuretic peptide (BNP), also the reduced left ventricular end-diastolic posterior wall thickness (LVPWd) and end-diastolic interventricular septal thickness (IVSd). Meanwhile, APN elevated miR-133a level which was downregulated by Ang II. To further investigate the underlying molecular mechanisms, we treated neonatal rat ventricular myocytes (NRVMs) with recombinant rat APN before Ang II stimulation. Pretreating cells with recombinant APN promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited ERK activation. By using the inhibitor of AMPK or a lentiviral vector expressing AMPK short hairpin RNA (shRNA) cancelled the positive effect of APN on miR-133a. The ERK inhibitor PD98059 reversed the downregulation of miR-133a induced by Ang II. These results indicated that the AMPK activation and ERK inhibition were responsible for the positive effect of APN on miR-133a. Furthermore, adiponectin receptor 1 (AdipoR1) mRNA expression was inhibited by Ang II stimulation. The positive effects of APN on AMPK activation and miR-133a, and the inhibitory effect on ERK phosphorylation were inhibited in NRVMs transfected with lentiviral AdipoR1shRNA. In addition, APN depressed the elevated expression of connective tissue growth factor (CTGF), a direct target of miR-133a, through the AMPK pathway. Taken together, our data indicated that APN reversed miR-133a levels through AMPK activation, reduced ERK1/2 phosphorylation in cardiomyocytes stimulated with Ang II, revealing a previously undemonstrated and important link between APN and miR-133a. |
| doi_str_mv | 10.1371/journal.pone.0148482 |
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However, whether APN has a potential effect on miR-133a remains unclear. In this study, we aimed to investigate whether APN could regulate miR-133a expression in Angiotensin II (Ang II) induced cardiac hypertrophy in vivo and in vitro. Lentiviral-mediated adiponectin treatment attenuated cardiac hypertrophy induced by Ang II infusion in male wistar rats as determined by reduced cell surface area and mRNA levels of atrial natriuretic peptide (ANF) and brain natriuretic peptide (BNP), also the reduced left ventricular end-diastolic posterior wall thickness (LVPWd) and end-diastolic interventricular septal thickness (IVSd). Meanwhile, APN elevated miR-133a level which was downregulated by Ang II. To further investigate the underlying molecular mechanisms, we treated neonatal rat ventricular myocytes (NRVMs) with recombinant rat APN before Ang II stimulation. Pretreating cells with recombinant APN promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited ERK activation. By using the inhibitor of AMPK or a lentiviral vector expressing AMPK short hairpin RNA (shRNA) cancelled the positive effect of APN on miR-133a. The ERK inhibitor PD98059 reversed the downregulation of miR-133a induced by Ang II. These results indicated that the AMPK activation and ERK inhibition were responsible for the positive effect of APN on miR-133a. Furthermore, adiponectin receptor 1 (AdipoR1) mRNA expression was inhibited by Ang II stimulation. The positive effects of APN on AMPK activation and miR-133a, and the inhibitory effect on ERK phosphorylation were inhibited in NRVMs transfected with lentiviral AdipoR1shRNA. In addition, APN depressed the elevated expression of connective tissue growth factor (CTGF), a direct target of miR-133a, through the AMPK pathway. Taken together, our data indicated that APN reversed miR-133a levels through AMPK activation, reduced ERK1/2 phosphorylation in cardiomyocytes stimulated with Ang II, revealing a previously undemonstrated and important link between APN and miR-133a.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0148482</identifier><identifier>PMID: 26845040</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Activation ; Adiponectin ; Adiponectin - genetics ; Adiponectin - metabolism ; AMP ; AMP-activated protein kinase ; AMP-Activated Protein Kinases - metabolism ; Angiogenesis ; Angiotensin ; Angiotensin II ; Angiotensin II - adverse effects ; Animals ; Apoptosis ; Atrial natriuretic peptide ; Biology and Life Sciences ; Brain ; Brain natriuretic peptide ; Cardiac muscle ; Cardiology ; Cardiomegaly - chemically induced ; Cardiomegaly - diagnosis ; Cardiomegaly - genetics ; Cardiomegaly - metabolism ; Cardiomyocytes ; Cardiovascular disease ; Cell growth ; Cell surface ; Connective tissue growth factor ; Connective Tissue Growth Factor - genetics ; Connective Tissue Growth Factor - metabolism ; Connective tissues ; Development and progression ; Diabetes ; Disease Models, Animal ; Echocardiography - methods ; Extracellular signal-regulated kinase ; Gene Expression ; Gene Expression Regulation ; Genetic aspects ; Genetic Vectors - genetics ; Growth factors ; Heart ; Heart diseases ; Heart failure ; Heart hypertrophy ; Hospitals ; Hypertension ; Hypertrophy ; Infusion ; Inhibition ; Inhibitors ; Kinases ; Lentivirus - genetics ; Male ; Medicine and Health Sciences ; MicroRNA ; MicroRNAs ; MicroRNAs - genetics ; Mitogen-Activated Protein Kinase 1 - metabolism ; Mitogen-Activated Protein Kinase 3 - metabolism ; Molecular modelling ; Myocytes ; Myocytes, Cardiac - metabolism ; Neonates ; Oxidation ; Pathology ; Peptide hormones ; Phosphorylation ; Physiological aspects ; Proteins ; Rats ; Receptors, Adiponectin - metabolism ; Regulators ; Research and Analysis Methods ; Ribonucleic acid ; RNA ; Rodents ; Signal Transduction ; Stimulation ; Surface area ; Transduction, Genetic ; Up-Regulation ; Ventricle ; Wall thickness ; Ying Li</subject><ispartof>PloS one, 2016-02, Vol.11 (2), p.e0148482-e0148482</ispartof><rights>COPYRIGHT 2016 Public Library of Science</rights><rights>2016 Li et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2016 Li et al 2016 Li et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c692t-77756ec8086a91ce982a9b7dc39242fba2075cce68dbaea4b7c6b0e5a7d94a293</citedby><cites>FETCH-LOGICAL-c692t-77756ec8086a91ce982a9b7dc39242fba2075cce68dbaea4b7c6b0e5a7d94a293</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741527/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC4741527/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26845040$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Karmazyn, Morris</contributor><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Cai, Xiaojun</creatorcontrib><creatorcontrib>Guan, Yuqing</creatorcontrib><creatorcontrib>Wang, Lei</creatorcontrib><creatorcontrib>Wang, Shuya</creatorcontrib><creatorcontrib>Li, Yueyan</creatorcontrib><creatorcontrib>Fu, Ying</creatorcontrib><creatorcontrib>Gao, Xiaoyuan</creatorcontrib><creatorcontrib>Su, Guohai</creatorcontrib><title>Adiponectin Upregulates MiR-133a in Cardiac Hypertrophy through AMPK Activation and Reduced ERK1/2 Phosphorylation</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Adiponectin and miR-133a are key regulators in cardiac hypertrophy. However, whether APN has a potential effect on miR-133a remains unclear. In this study, we aimed to investigate whether APN could regulate miR-133a expression in Angiotensin II (Ang II) induced cardiac hypertrophy in vivo and in vitro. Lentiviral-mediated adiponectin treatment attenuated cardiac hypertrophy induced by Ang II infusion in male wistar rats as determined by reduced cell surface area and mRNA levels of atrial natriuretic peptide (ANF) and brain natriuretic peptide (BNP), also the reduced left ventricular end-diastolic posterior wall thickness (LVPWd) and end-diastolic interventricular septal thickness (IVSd). Meanwhile, APN elevated miR-133a level which was downregulated by Ang II. To further investigate the underlying molecular mechanisms, we treated neonatal rat ventricular myocytes (NRVMs) with recombinant rat APN before Ang II stimulation. Pretreating cells with recombinant APN promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited ERK activation. By using the inhibitor of AMPK or a lentiviral vector expressing AMPK short hairpin RNA (shRNA) cancelled the positive effect of APN on miR-133a. The ERK inhibitor PD98059 reversed the downregulation of miR-133a induced by Ang II. These results indicated that the AMPK activation and ERK inhibition were responsible for the positive effect of APN on miR-133a. Furthermore, adiponectin receptor 1 (AdipoR1) mRNA expression was inhibited by Ang II stimulation. The positive effects of APN on AMPK activation and miR-133a, and the inhibitory effect on ERK phosphorylation were inhibited in NRVMs transfected with lentiviral AdipoR1shRNA. In addition, APN depressed the elevated expression of connective tissue growth factor (CTGF), a direct target of miR-133a, through the AMPK pathway. Taken together, our data indicated that APN reversed miR-133a levels through AMPK activation, reduced ERK1/2 phosphorylation in cardiomyocytes stimulated with Ang II, revealing a previously undemonstrated and important link between APN and miR-133a.</description><subject>Activation</subject><subject>Adiponectin</subject><subject>Adiponectin - genetics</subject><subject>Adiponectin - metabolism</subject><subject>AMP</subject><subject>AMP-activated protein kinase</subject><subject>AMP-Activated Protein Kinases - metabolism</subject><subject>Angiogenesis</subject><subject>Angiotensin</subject><subject>Angiotensin II</subject><subject>Angiotensin II - adverse effects</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Atrial natriuretic peptide</subject><subject>Biology and Life Sciences</subject><subject>Brain</subject><subject>Brain natriuretic peptide</subject><subject>Cardiac muscle</subject><subject>Cardiology</subject><subject>Cardiomegaly - chemically induced</subject><subject>Cardiomegaly - diagnosis</subject><subject>Cardiomegaly - genetics</subject><subject>Cardiomegaly - metabolism</subject><subject>Cardiomyocytes</subject><subject>Cardiovascular disease</subject><subject>Cell growth</subject><subject>Cell surface</subject><subject>Connective tissue growth factor</subject><subject>Connective Tissue Growth Factor - genetics</subject><subject>Connective Tissue Growth Factor - metabolism</subject><subject>Connective tissues</subject><subject>Development and progression</subject><subject>Diabetes</subject><subject>Disease Models, Animal</subject><subject>Echocardiography - methods</subject><subject>Extracellular signal-regulated kinase</subject><subject>Gene Expression</subject><subject>Gene Expression Regulation</subject><subject>Genetic aspects</subject><subject>Genetic Vectors - genetics</subject><subject>Growth factors</subject><subject>Heart</subject><subject>Heart diseases</subject><subject>Heart failure</subject><subject>Heart hypertrophy</subject><subject>Hospitals</subject><subject>Hypertension</subject><subject>Hypertrophy</subject><subject>Infusion</subject><subject>Inhibition</subject><subject>Inhibitors</subject><subject>Kinases</subject><subject>Lentivirus - genetics</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>MicroRNA</subject><subject>MicroRNAs</subject><subject>MicroRNAs - genetics</subject><subject>Mitogen-Activated Protein Kinase 1 - metabolism</subject><subject>Mitogen-Activated Protein Kinase 3 - metabolism</subject><subject>Molecular modelling</subject><subject>Myocytes</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Neonates</subject><subject>Oxidation</subject><subject>Pathology</subject><subject>Peptide hormones</subject><subject>Phosphorylation</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Rats</subject><subject>Receptors, Adiponectin - metabolism</subject><subject>Regulators</subject><subject>Research and Analysis Methods</subject><subject>Ribonucleic acid</subject><subject>RNA</subject><subject>Rodents</subject><subject>Signal Transduction</subject><subject>Stimulation</subject><subject>Surface area</subject><subject>Transduction, Genetic</subject><subject>Up-Regulation</subject><subject>Ventricle</subject><subject>Wall thickness</subject><subject>Ying Li</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</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><sourceid>DOA</sourceid><recordid>eNqNk9Fu0zAUhiMEYmPwBggiISG4aGc7jp3cIFXVYNU2bSqMW-vEdhpXaZzZyUTfHnfNpgbtAvnC1vH3_7aPz4mi9xhNccLx6dr2roF62tpGTxGmGc3Ii-gY5wmZMIKSlwfro-iN92uE0iRj7HV0RFhGU0TRceRmyuwcZGea-LZ1etXX0GkfX5nlBCcJxCE-B6cMyPh822rXOdtW27irnO1XVTy7urmIZ0F-D52xTQyNipda9VKr-Gx5gU9JfFNZ31bWbesH5G30qoTa63fDfBLdfj_7NT-fXF7_WMxnlxPJctJNOOcp0zJDGYMcS51nBPKCK5nkhJKyAIJ4KqVmmSpAAy24ZAXSKXCVUyB5chJ93Pu2tfViSJcXmDPCeEowC8RiTygLa9E6swG3FRaMeAhYtxLgOiNrLRAUgFKuKICkEooch8uUSOlcIYSSInh9G07ri41WUjedg3pkOt5pTCVW9l5QTnFKeDD4Mhg4e9dr34mN8VLXNTTa9vt75yxLMQrop3_Q5183UCsIDzBNacO5cmcqZpSSJEtpSgM1fYYKQ-mNkaEyShPiI8HXkSAwnf7TraD3Xix-Lv-fvf49Zj8fsJWGuqu8rftdyfgxSPegdNZ7p8unJGMkdq3xmA2xK2wxtEaQfTj8oCfRYy8kfwFNYQlX</recordid><startdate>20160204</startdate><enddate>20160204</enddate><creator>Li, Ying</creator><creator>Cai, Xiaojun</creator><creator>Guan, Yuqing</creator><creator>Wang, Lei</creator><creator>Wang, Shuya</creator><creator>Li, Yueyan</creator><creator>Fu, Ying</creator><creator>Gao, Xiaoyuan</creator><creator>Su, Guohai</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</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>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope></search><sort><creationdate>20160204</creationdate><title>Adiponectin Upregulates MiR-133a in Cardiac Hypertrophy through AMPK Activation and Reduced ERK1/2 Phosphorylation</title><author>Li, Ying ; Cai, Xiaojun ; Guan, Yuqing ; Wang, Lei ; Wang, Shuya ; Li, Yueyan ; Fu, Ying ; Gao, Xiaoyuan ; Su, Guohai</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c692t-77756ec8086a91ce982a9b7dc39242fba2075cce68dbaea4b7c6b0e5a7d94a293</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Activation</topic><topic>Adiponectin</topic><topic>Adiponectin - genetics</topic><topic>Adiponectin - metabolism</topic><topic>AMP</topic><topic>AMP-activated protein kinase</topic><topic>AMP-Activated Protein Kinases - metabolism</topic><topic>Angiogenesis</topic><topic>Angiotensin</topic><topic>Angiotensin II</topic><topic>Angiotensin II - adverse effects</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Atrial natriuretic peptide</topic><topic>Biology and Life Sciences</topic><topic>Brain</topic><topic>Brain natriuretic peptide</topic><topic>Cardiac muscle</topic><topic>Cardiology</topic><topic>Cardiomegaly - chemically induced</topic><topic>Cardiomegaly - diagnosis</topic><topic>Cardiomegaly - genetics</topic><topic>Cardiomegaly - metabolism</topic><topic>Cardiomyocytes</topic><topic>Cardiovascular disease</topic><topic>Cell growth</topic><topic>Cell surface</topic><topic>Connective tissue growth factor</topic><topic>Connective Tissue Growth Factor - genetics</topic><topic>Connective Tissue Growth Factor - metabolism</topic><topic>Connective tissues</topic><topic>Development and progression</topic><topic>Diabetes</topic><topic>Disease Models, Animal</topic><topic>Echocardiography - 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metabolism</topic><topic>Regulators</topic><topic>Research and Analysis Methods</topic><topic>Ribonucleic acid</topic><topic>RNA</topic><topic>Rodents</topic><topic>Signal Transduction</topic><topic>Stimulation</topic><topic>Surface area</topic><topic>Transduction, Genetic</topic><topic>Up-Regulation</topic><topic>Ventricle</topic><topic>Wall thickness</topic><topic>Ying Li</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Cai, Xiaojun</creatorcontrib><creatorcontrib>Guan, Yuqing</creatorcontrib><creatorcontrib>Wang, Lei</creatorcontrib><creatorcontrib>Wang, Shuya</creatorcontrib><creatorcontrib>Li, Yueyan</creatorcontrib><creatorcontrib>Fu, Ying</creatorcontrib><creatorcontrib>Gao, Xiaoyuan</creatorcontrib><creatorcontrib>Su, Guohai</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Gale In Context: Opposing Viewpoints</collection><collection>Gale In Context: Science</collection><collection>ProQuest Central (Corporate)</collection><collection>Animal Behavior Abstracts</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Biotechnology Research Abstracts</collection><collection>Nursing & Allied Health Database</collection><collection>Ecology Abstracts</collection><collection>Entomology Abstracts (Full archive)</collection><collection>Immunology Abstracts</collection><collection>Meteorological & Geoastrophysical Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Agricultural Science Collection</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>Public Health Database</collection><collection>Technology Research Database</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Technology 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>Materials Science & Engineering Collection</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>Advanced Technologies & Aerospace Collection</collection><collection>Agricultural & Environmental Science Collection</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Technology Collection</collection><collection>Natural Science Collection</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>ProQuest Materials Science Collection</collection><collection>ProQuest Central Korea</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Materials Science Database</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Meteorological & Geoastrophysical Abstracts - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Ying</au><au>Cai, Xiaojun</au><au>Guan, Yuqing</au><au>Wang, Lei</au><au>Wang, Shuya</au><au>Li, Yueyan</au><au>Fu, Ying</au><au>Gao, Xiaoyuan</au><au>Su, Guohai</au><au>Karmazyn, Morris</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Adiponectin Upregulates MiR-133a in Cardiac Hypertrophy through AMPK Activation and Reduced ERK1/2 Phosphorylation</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2016-02-04</date><risdate>2016</risdate><volume>11</volume><issue>2</issue><spage>e0148482</spage><epage>e0148482</epage><pages>e0148482-e0148482</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Adiponectin and miR-133a are key regulators in cardiac hypertrophy. However, whether APN has a potential effect on miR-133a remains unclear. In this study, we aimed to investigate whether APN could regulate miR-133a expression in Angiotensin II (Ang II) induced cardiac hypertrophy in vivo and in vitro. Lentiviral-mediated adiponectin treatment attenuated cardiac hypertrophy induced by Ang II infusion in male wistar rats as determined by reduced cell surface area and mRNA levels of atrial natriuretic peptide (ANF) and brain natriuretic peptide (BNP), also the reduced left ventricular end-diastolic posterior wall thickness (LVPWd) and end-diastolic interventricular septal thickness (IVSd). Meanwhile, APN elevated miR-133a level which was downregulated by Ang II. To further investigate the underlying molecular mechanisms, we treated neonatal rat ventricular myocytes (NRVMs) with recombinant rat APN before Ang II stimulation. Pretreating cells with recombinant APN promoted AMP-activated protein kinase (AMPK) phosphorylation and inhibited ERK activation. By using the inhibitor of AMPK or a lentiviral vector expressing AMPK short hairpin RNA (shRNA) cancelled the positive effect of APN on miR-133a. The ERK inhibitor PD98059 reversed the downregulation of miR-133a induced by Ang II. These results indicated that the AMPK activation and ERK inhibition were responsible for the positive effect of APN on miR-133a. Furthermore, adiponectin receptor 1 (AdipoR1) mRNA expression was inhibited by Ang II stimulation. The positive effects of APN on AMPK activation and miR-133a, and the inhibitory effect on ERK phosphorylation were inhibited in NRVMs transfected with lentiviral AdipoR1shRNA. In addition, APN depressed the elevated expression of connective tissue growth factor (CTGF), a direct target of miR-133a, through the AMPK pathway. Taken together, our data indicated that APN reversed miR-133a levels through AMPK activation, reduced ERK1/2 phosphorylation in cardiomyocytes stimulated with Ang II, revealing a previously undemonstrated and important link between APN and miR-133a.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>26845040</pmid><doi>10.1371/journal.pone.0148482</doi><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2016-02, Vol.11 (2), p.e0148482-e0148482 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_1762675216 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS); PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Activation Adiponectin Adiponectin - genetics Adiponectin - metabolism AMP AMP-activated protein kinase AMP-Activated Protein Kinases - metabolism Angiogenesis Angiotensin Angiotensin II Angiotensin II - adverse effects Animals Apoptosis Atrial natriuretic peptide Biology and Life Sciences Brain Brain natriuretic peptide Cardiac muscle Cardiology Cardiomegaly - chemically induced Cardiomegaly - diagnosis Cardiomegaly - genetics Cardiomegaly - metabolism Cardiomyocytes Cardiovascular disease Cell growth Cell surface Connective tissue growth factor Connective Tissue Growth Factor - genetics Connective Tissue Growth Factor - metabolism Connective tissues Development and progression Diabetes Disease Models, Animal Echocardiography - methods Extracellular signal-regulated kinase Gene Expression Gene Expression Regulation Genetic aspects Genetic Vectors - genetics Growth factors Heart Heart diseases Heart failure Heart hypertrophy Hospitals Hypertension Hypertrophy Infusion Inhibition Inhibitors Kinases Lentivirus - genetics Male Medicine and Health Sciences MicroRNA MicroRNAs MicroRNAs - genetics Mitogen-Activated Protein Kinase 1 - metabolism Mitogen-Activated Protein Kinase 3 - metabolism Molecular modelling Myocytes Myocytes, Cardiac - metabolism Neonates Oxidation Pathology Peptide hormones Phosphorylation Physiological aspects Proteins Rats Receptors, Adiponectin - metabolism Regulators Research and Analysis Methods Ribonucleic acid RNA Rodents Signal Transduction Stimulation Surface area Transduction, Genetic Up-Regulation Ventricle Wall thickness Ying Li |
| title | Adiponectin Upregulates MiR-133a in Cardiac Hypertrophy through AMPK Activation and Reduced ERK1/2 Phosphorylation |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-21T03%3A30%3A24IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Adiponectin%20Upregulates%20MiR-133a%20in%20Cardiac%20Hypertrophy%20through%20AMPK%20Activation%20and%20Reduced%20ERK1/2%20Phosphorylation&rft.jtitle=PloS%20one&rft.au=Li,%20Ying&rft.date=2016-02-04&rft.volume=11&rft.issue=2&rft.spage=e0148482&rft.epage=e0148482&rft.pages=e0148482-e0148482&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0148482&rft_dat=%3Cgale_plos_%3EA442385454%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1762675216&rft_id=info:pmid/26845040&rft_galeid=A442385454&rft_doaj_id=oai_doaj_org_article_0aba057d4aac4cab91a9bf0de9d0003b&rfr_iscdi=true |