Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury
Objective. This study aimed to investigate whether the nonselective A2 adenosine receptor agonist NECA induces cardioprotection against myocardial ischemia/reperfusion (I/R) injury via glycogen synthase kinase 3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP) through inhibition o...
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| Veröffentlicht in: | Oxidative medicine and cellular longevity 2017-01, Vol.2017 (2017), p.1-10 |
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| creator | Xi, Jinkun Jing, Liwei Zhang, Yidong He, Yonggui Han, Hui Xing, Fengmei Xu, Zhelong |
| description | Objective. This study aimed to investigate whether the nonselective A2 adenosine receptor agonist NECA induces cardioprotection against myocardial ischemia/reperfusion (I/R) injury via glycogen synthase kinase 3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP) through inhibition of endoplasmic reticulum stress (ERS). Methods and Results. H9c2 cells were exposed to H2O2 for 20 minutes. NECA significantly prevented H2O2-induced TMRE fluorescence reduction, indicating that NECA inhibited the mPTP opening. NECA blocked H2O2-induced GSK-3β phosphorylation and GRP94 expression. NECA increased GSK-3β phosphorylation and decreased GRP94 expression, which were prevented by both ERS inductor 2-DG and PKG inhibitor KT5823, suggesting that NECA may induce cardioprotection through GSK-3β and cGMP/PKG via ERS. In isolated rat hearts, both NECA and the ERS inhibitor TUDCA decreased myocardial infarction, increased GSK-3β phosphorylation, and reversed GRP94 expression at reperfusion, suggesting that NECA protected the heart by inhibiting GSK-3β and ERS. Transmission electron microscopy showed that NECA and TUDCA reduced mitochondrial swelling and endoplasmic reticulum expansion, further supporting that NECA protected the heart by preventing the mPTP opening and ERS. Conclusion. These data suggest that NECA prevents the mPTP opening through inactivation of GSK-3β via ERS inhibition. The cGMP/PKG signaling pathway is responsible for GSK-3β inactivation by NECA. |
| doi_str_mv | 10.1155/2017/2490501 |
| format | Article |
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This study aimed to investigate whether the nonselective A2 adenosine receptor agonist NECA induces cardioprotection against myocardial ischemia/reperfusion (I/R) injury via glycogen synthase kinase 3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP) through inhibition of endoplasmic reticulum stress (ERS). Methods and Results. H9c2 cells were exposed to H2O2 for 20 minutes. NECA significantly prevented H2O2-induced TMRE fluorescence reduction, indicating that NECA inhibited the mPTP opening. NECA blocked H2O2-induced GSK-3β phosphorylation and GRP94 expression. NECA increased GSK-3β phosphorylation and decreased GRP94 expression, which were prevented by both ERS inductor 2-DG and PKG inhibitor KT5823, suggesting that NECA may induce cardioprotection through GSK-3β and cGMP/PKG via ERS. In isolated rat hearts, both NECA and the ERS inhibitor TUDCA decreased myocardial infarction, increased GSK-3β phosphorylation, and reversed GRP94 expression at reperfusion, suggesting that NECA protected the heart by inhibiting GSK-3β and ERS. Transmission electron microscopy showed that NECA and TUDCA reduced mitochondrial swelling and endoplasmic reticulum expansion, further supporting that NECA protected the heart by preventing the mPTP opening and ERS. Conclusion. These data suggest that NECA prevents the mPTP opening through inactivation of GSK-3β via ERS inhibition. The cGMP/PKG signaling pathway is responsible for GSK-3β inactivation by NECA.</description><identifier>ISSN: 1942-0900</identifier><identifier>EISSN: 1942-0994</identifier><identifier>DOI: 10.1155/2017/2490501</identifier><identifier>PMID: 29391923</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Adenosine ; Adenosine-5'-(N-ethylcarboxamide) - pharmacology ; Animals ; Apoptosis ; Cardiomyocytes ; Cardiotonic Agents - pharmacology ; Endoplasmic reticulum ; Endoplasmic Reticulum Stress - drug effects ; Endoplasmic Reticulum Stress - physiology ; Glycogen ; Glycogen Synthase Kinase 3 beta - metabolism ; Heart ; Hydrogen Peroxide - administration & dosage ; Ischemia ; Kinases ; Laboratory animals ; Male ; Mitochondrial Membrane Transport Proteins - metabolism ; Mitochondrial Permeability Transition Pore ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - prevention & control ; Ostomy ; Oxidative stress ; Permeability ; Phosphorylation ; Physiology ; Proteins ; Rats ; Rodents ; Roles ; Signal Transduction - drug effects ; Synthesis</subject><ispartof>Oxidative medicine and cellular longevity, 2017-01, Vol.2017 (2017), p.1-10</ispartof><rights>Copyright © 2017 Fengmei Xing et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2017 Fengmei Xing et al.; This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.</rights><rights>Copyright © 2017 Fengmei Xing et al. 2017</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-b20dcfb232cb7be0ce8bfab535ddf999ba4c8a61076b10973fe5c6724fe367fc3</citedby><cites>FETCH-LOGICAL-c499t-b20dcfb232cb7be0ce8bfab535ddf999ba4c8a61076b10973fe5c6724fe367fc3</cites><orcidid>0000-0002-5220-1192</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/PMC5748120/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5748120/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27929,27930,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29391923$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Li, Haobo</contributor><creatorcontrib>Xi, Jinkun</creatorcontrib><creatorcontrib>Jing, Liwei</creatorcontrib><creatorcontrib>Zhang, Yidong</creatorcontrib><creatorcontrib>He, Yonggui</creatorcontrib><creatorcontrib>Han, Hui</creatorcontrib><creatorcontrib>Xing, Fengmei</creatorcontrib><creatorcontrib>Xu, Zhelong</creatorcontrib><title>Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury</title><title>Oxidative medicine and cellular longevity</title><addtitle>Oxid Med Cell Longev</addtitle><description>Objective. This study aimed to investigate whether the nonselective A2 adenosine receptor agonist NECA induces cardioprotection against myocardial ischemia/reperfusion (I/R) injury via glycogen synthase kinase 3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP) through inhibition of endoplasmic reticulum stress (ERS). Methods and Results. H9c2 cells were exposed to H2O2 for 20 minutes. NECA significantly prevented H2O2-induced TMRE fluorescence reduction, indicating that NECA inhibited the mPTP opening. NECA blocked H2O2-induced GSK-3β phosphorylation and GRP94 expression. NECA increased GSK-3β phosphorylation and decreased GRP94 expression, which were prevented by both ERS inductor 2-DG and PKG inhibitor KT5823, suggesting that NECA may induce cardioprotection through GSK-3β and cGMP/PKG via ERS. In isolated rat hearts, both NECA and the ERS inhibitor TUDCA decreased myocardial infarction, increased GSK-3β phosphorylation, and reversed GRP94 expression at reperfusion, suggesting that NECA protected the heart by inhibiting GSK-3β and ERS. Transmission electron microscopy showed that NECA and TUDCA reduced mitochondrial swelling and endoplasmic reticulum expansion, further supporting that NECA protected the heart by preventing the mPTP opening and ERS. Conclusion. These data suggest that NECA prevents the mPTP opening through inactivation of GSK-3β via ERS inhibition. The cGMP/PKG signaling pathway is responsible for GSK-3β inactivation by NECA.</description><subject>Adenosine</subject><subject>Adenosine-5'-(N-ethylcarboxamide) - pharmacology</subject><subject>Animals</subject><subject>Apoptosis</subject><subject>Cardiomyocytes</subject><subject>Cardiotonic Agents - pharmacology</subject><subject>Endoplasmic reticulum</subject><subject>Endoplasmic Reticulum Stress - drug effects</subject><subject>Endoplasmic Reticulum Stress - physiology</subject><subject>Glycogen</subject><subject>Glycogen Synthase Kinase 3 beta - metabolism</subject><subject>Heart</subject><subject>Hydrogen Peroxide - administration & dosage</subject><subject>Ischemia</subject><subject>Kinases</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Mitochondrial Membrane Transport Proteins - metabolism</subject><subject>Mitochondrial Permeability Transition Pore</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - prevention & control</subject><subject>Ostomy</subject><subject>Oxidative stress</subject><subject>Permeability</subject><subject>Phosphorylation</subject><subject>Physiology</subject><subject>Proteins</subject><subject>Rats</subject><subject>Rodents</subject><subject>Roles</subject><subject>Signal Transduction - drug effects</subject><subject>Synthesis</subject><issn>1942-0900</issn><issn>1942-0994</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>8G5</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>GUQSH</sourceid><sourceid>M2O</sourceid><recordid>eNqNkk2rEzEUhgdRvB-6cy0Bl96x-ZrJZCOUUrVwUai6DknmpE2ZScZkRrn_3imtvbpzdQ6ch4cX3lMUrwh-R0hVLSgmYkG5xBUmT4prIjktsZT86WXH-Kq4yfmAcc0oJ8-LKyqZJJKy6-KwjR1kFB1ahzYOnc69t2gLo7dTN_Xo65ggZ-QD-rxeLctNaCcLLVrp1Po4pDiCHX0MSO-0D3lEm2z30Hu92MIAyU35eNyEw5QeXhTPnO4yvDzP2-L7h_W31afy_svHzWp5X1ou5VgailvrDGXUGmEAW2iM06ZiVds6KaXR3Da6JljUhmApmIPK1oJyB6wWzrLb4v3JO0ymh9ZCGJPu1JB8r9ODitqrfy_B79Uu_lSV4A2heBa8OQtS_DFBHtUhTinMmRWRDeNcskY-UjvdgfLBxVlme5-tWtaYCiJYI2bq7kTZFHNO4C45CFbH_tSxP3Xub8Zf_539Av8pbAbenoC9D63-5f9TBzMDTj_S82vghrLf4uut9g</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Xi, Jinkun</creator><creator>Jing, Liwei</creator><creator>Zhang, Yidong</creator><creator>He, Yonggui</creator><creator>Han, Hui</creator><creator>Xing, Fengmei</creator><creator>Xu, Zhelong</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>8G5</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>GUQSH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>M2O</scope><scope>MBDVC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-5220-1192</orcidid></search><sort><creationdate>20170101</creationdate><title>Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury</title><author>Xi, Jinkun ; Jing, Liwei ; Zhang, Yidong ; He, Yonggui ; Han, Hui ; Xing, Fengmei ; Xu, Zhelong</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-b20dcfb232cb7be0ce8bfab535ddf999ba4c8a61076b10973fe5c6724fe367fc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adenosine</topic><topic>Adenosine-5'-(N-ethylcarboxamide) - pharmacology</topic><topic>Animals</topic><topic>Apoptosis</topic><topic>Cardiomyocytes</topic><topic>Cardiotonic Agents - pharmacology</topic><topic>Endoplasmic reticulum</topic><topic>Endoplasmic Reticulum Stress - drug effects</topic><topic>Endoplasmic Reticulum Stress - physiology</topic><topic>Glycogen</topic><topic>Glycogen Synthase Kinase 3 beta - metabolism</topic><topic>Heart</topic><topic>Hydrogen Peroxide - administration & dosage</topic><topic>Ischemia</topic><topic>Kinases</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Mitochondrial Membrane Transport Proteins - metabolism</topic><topic>Mitochondrial Permeability Transition Pore</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - prevention & control</topic><topic>Ostomy</topic><topic>Oxidative stress</topic><topic>Permeability</topic><topic>Phosphorylation</topic><topic>Physiology</topic><topic>Proteins</topic><topic>Rats</topic><topic>Rodents</topic><topic>Roles</topic><topic>Signal Transduction - drug effects</topic><topic>Synthesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Xi, Jinkun</creatorcontrib><creatorcontrib>Jing, Liwei</creatorcontrib><creatorcontrib>Zhang, Yidong</creatorcontrib><creatorcontrib>He, Yonggui</creatorcontrib><creatorcontrib>Han, Hui</creatorcontrib><creatorcontrib>Xing, Fengmei</creatorcontrib><creatorcontrib>Xu, Zhelong</creatorcontrib><collection>الدوريات العلمية والإحصائية - e-Marefa Academic and Statistical Periodicals</collection><collection>معرفة - المحتوى العربي الأكاديمي المتكامل - e-Marefa Academic Complete</collection><collection>Hindawi Publishing Complete</collection><collection>Hindawi Publishing Subscription Journals</collection><collection>Hindawi Publishing Open Access</collection><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>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>Research Library (Alumni Edition)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</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>Research Library Prep</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Research Library</collection><collection>Research Library (Corporate)</collection><collection>Access via ProQuest (Open Access)</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>ProQuest Central Basic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oxidative medicine and cellular longevity</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Xi, Jinkun</au><au>Jing, Liwei</au><au>Zhang, Yidong</au><au>He, Yonggui</au><au>Han, Hui</au><au>Xing, Fengmei</au><au>Xu, Zhelong</au><au>Li, Haobo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury</atitle><jtitle>Oxidative medicine and cellular longevity</jtitle><addtitle>Oxid Med Cell Longev</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>2017</volume><issue>2017</issue><spage>1</spage><epage>10</epage><pages>1-10</pages><issn>1942-0900</issn><eissn>1942-0994</eissn><abstract>Objective. This study aimed to investigate whether the nonselective A2 adenosine receptor agonist NECA induces cardioprotection against myocardial ischemia/reperfusion (I/R) injury via glycogen synthase kinase 3β (GSK-3β) and the mitochondrial permeability transition pore (mPTP) through inhibition of endoplasmic reticulum stress (ERS). Methods and Results. H9c2 cells were exposed to H2O2 for 20 minutes. NECA significantly prevented H2O2-induced TMRE fluorescence reduction, indicating that NECA inhibited the mPTP opening. NECA blocked H2O2-induced GSK-3β phosphorylation and GRP94 expression. NECA increased GSK-3β phosphorylation and decreased GRP94 expression, which were prevented by both ERS inductor 2-DG and PKG inhibitor KT5823, suggesting that NECA may induce cardioprotection through GSK-3β and cGMP/PKG via ERS. In isolated rat hearts, both NECA and the ERS inhibitor TUDCA decreased myocardial infarction, increased GSK-3β phosphorylation, and reversed GRP94 expression at reperfusion, suggesting that NECA protected the heart by inhibiting GSK-3β and ERS. Transmission electron microscopy showed that NECA and TUDCA reduced mitochondrial swelling and endoplasmic reticulum expansion, further supporting that NECA protected the heart by preventing the mPTP opening and ERS. Conclusion. These data suggest that NECA prevents the mPTP opening through inactivation of GSK-3β via ERS inhibition. The cGMP/PKG signaling pathway is responsible for GSK-3β inactivation by NECA.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>29391923</pmid><doi>10.1155/2017/2490501</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-5220-1192</orcidid><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; PubMed Central Open Access; Wiley Online Library (Open Access Collection); PubMed Central; Alma/SFX Local Collection |
| subjects | Adenosine Adenosine-5'-(N-ethylcarboxamide) - pharmacology Animals Apoptosis Cardiomyocytes Cardiotonic Agents - pharmacology Endoplasmic reticulum Endoplasmic Reticulum Stress - drug effects Endoplasmic Reticulum Stress - physiology Glycogen Glycogen Synthase Kinase 3 beta - metabolism Heart Hydrogen Peroxide - administration & dosage Ischemia Kinases Laboratory animals Male Mitochondrial Membrane Transport Proteins - metabolism Mitochondrial Permeability Transition Pore Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - prevention & control Ostomy Oxidative stress Permeability Phosphorylation Physiology Proteins Rats Rodents Roles Signal Transduction - drug effects Synthesis |
| title | Roles of Endoplasmic Reticulum Stress in NECA-Induced Cardioprotection against Ischemia/Reperfusion Injury |
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