Cardioprotection of ischaemic preconditioning is associated with inhibition of translocation of MLKL within the plasma membrane
Necroptosis, a form of cell loss involving the RIP1‐RIP3‐MLKL axis, has been identified in cardiac pathologies while its inhibition is cardioprotective. We investigated whether the improvement of heart function because of ischaemic preconditioning is associated with mitigation of necroptotic signali...
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| Veröffentlicht in: | Journal of cellular and molecular medicine 2018-09, Vol.22 (9), p.4183-4196 |
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| creator | Szobi, Adrián Farkašová‐Ledvényiová, Veronika Lichý, Martin Muráriková, Martina Čarnická, Slávka Ravingerová, Tatiana Adameová, Adriana |
| description | Necroptosis, a form of cell loss involving the RIP1‐RIP3‐MLKL axis, has been identified in cardiac pathologies while its inhibition is cardioprotective. We investigated whether the improvement of heart function because of ischaemic preconditioning is associated with mitigation of necroptotic signaling, and these effects were compared with a pharmacological antinecroptotic approach targeting RIP1. Langendorff‐perfused rat hearts were subjected to ischaemic preconditioning with or without a RIP1 inhibitor (Nec‐1s). Necroptotic signaling and the assessment of oxidative damage and a putative involvement of CaMKII in this process were analysed in whole tissue and subcellular fractions. Ischaemic preconditioning, Nec‐1s and their combination improved postischaemic heart function recovery and reduced infarct size to a similar degree what was in line with the prevention of MLKL oligomerization and translocation to the membrane. On the other hand, membrane peroxidation and apoptosis were unchanged by either approach. Ischaemic preconditioning failed to ameliorate ischaemia–reperfusion‐induced increase in RIP1 and RIP3 while pSer229‐RIP3 levels were reduced only by Nec‐1s. In spite of the additive phosphorylation of CaMKII and PLN because of ditherapy, the postischaemic contractile force and relaxation was comparably improved in all the intervention groups while antiarrhythmic effects were observed in the ischaemic preconditioning group only. Necroptosis inhibition seems to be involved in cardioprotection of ischaemic preconditioning and is comparable but not intensified by an anti‐RIP1 agent. Changes in oxidative stress nor CaMKII signaling are unlikely to explain the beneficial effects. |
| doi_str_mv | 10.1111/jcmm.13697 |
| format | Article |
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We investigated whether the improvement of heart function because of ischaemic preconditioning is associated with mitigation of necroptotic signaling, and these effects were compared with a pharmacological antinecroptotic approach targeting RIP1. Langendorff‐perfused rat hearts were subjected to ischaemic preconditioning with or without a RIP1 inhibitor (Nec‐1s). Necroptotic signaling and the assessment of oxidative damage and a putative involvement of CaMKII in this process were analysed in whole tissue and subcellular fractions. Ischaemic preconditioning, Nec‐1s and their combination improved postischaemic heart function recovery and reduced infarct size to a similar degree what was in line with the prevention of MLKL oligomerization and translocation to the membrane. On the other hand, membrane peroxidation and apoptosis were unchanged by either approach. Ischaemic preconditioning failed to ameliorate ischaemia–reperfusion‐induced increase in RIP1 and RIP3 while pSer229‐RIP3 levels were reduced only by Nec‐1s. In spite of the additive phosphorylation of CaMKII and PLN because of ditherapy, the postischaemic contractile force and relaxation was comparably improved in all the intervention groups while antiarrhythmic effects were observed in the ischaemic preconditioning group only. Necroptosis inhibition seems to be involved in cardioprotection of ischaemic preconditioning and is comparable but not intensified by an anti‐RIP1 agent. Changes in oxidative stress nor CaMKII signaling are unlikely to explain the beneficial effects.</description><identifier>ISSN: 1582-1838</identifier><identifier>EISSN: 1582-4934</identifier><identifier>DOI: 10.1111/jcmm.13697</identifier><identifier>PMID: 29921042</identifier><language>eng</language><publisher>England: John Wiley & Sons, Inc</publisher><subject>Animals ; Anti-Arrhythmia Agents - pharmacology ; Apoptosis ; Apoptosis - drug effects ; Ca2+/calmodulin-dependent protein kinase II ; Calcium-Binding Proteins - genetics ; Calcium-Binding Proteins - metabolism ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics ; Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism ; Cell Membrane - drug effects ; Cell Membrane - metabolism ; Gene Expression Regulation ; Heart ; Heart - drug effects ; Heart - physiopathology ; Heart function ; Imidazoles - pharmacology ; Indoles - pharmacology ; Inhibition ; ischaemia‐reperfusion injury ; Ischemia ; Ischemic Preconditioning, Myocardial ; Male ; Muscle contraction ; Myocardial Reperfusion Injury - genetics ; Myocardial Reperfusion Injury - metabolism ; Myocardial Reperfusion Injury - pathology ; Myocardial Reperfusion Injury - therapy ; Myocytes, Cardiac - drug effects ; Myocytes, Cardiac - metabolism ; Myocytes, Cardiac - pathology ; Necroptosis ; Necrosis - genetics ; Necrosis - metabolism ; Necrosis - pathology ; Necrosis - prevention & control ; Oligomerization ; Organ Culture Techniques ; Original ; Oxidative Stress ; Peroxidation ; Phosphorylation ; Phosphorylation - drug effects ; Preconditioning ; Protein Kinases - genetics ; Protein Kinases - metabolism ; Protein Serine-Threonine Kinases - antagonists & inhibitors ; Protein Serine-Threonine Kinases - genetics ; Protein Serine-Threonine Kinases - metabolism ; Protein Transport - drug effects ; Rats ; Rats, Wistar ; Receptor-Interacting Protein Serine-Threonine Kinases - genetics ; Receptor-Interacting Protein Serine-Threonine Kinases - metabolism ; Reperfusion ; RIP1 inhibition ; Signal Transduction ; Translocation</subject><ispartof>Journal of cellular and molecular medicine, 2018-09, Vol.22 (9), p.4183-4196</ispartof><rights>2018 Comenius University in Bratislava, Faculty of Pharmacy. Journal of Cellular and Molecular Medicine published by John Wiley & Sons Ltd and Foundation for Cellular and Molecular Medicine.</rights><rights>2018. This work is published under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4487-bf653cf5e93176240658c6f55023cc5c8ff7e346c68c537176e557bce610512a3</citedby><cites>FETCH-LOGICAL-c4487-bf653cf5e93176240658c6f55023cc5c8ff7e346c68c537176e557bce610512a3</cites><orcidid>0000-0002-9803-043X</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/PMC6111849/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6111849/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,865,886,1418,11567,27929,27930,45579,45580,46057,46481,53796,53798</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29921042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Szobi, Adrián</creatorcontrib><creatorcontrib>Farkašová‐Ledvényiová, Veronika</creatorcontrib><creatorcontrib>Lichý, Martin</creatorcontrib><creatorcontrib>Muráriková, Martina</creatorcontrib><creatorcontrib>Čarnická, Slávka</creatorcontrib><creatorcontrib>Ravingerová, Tatiana</creatorcontrib><creatorcontrib>Adameová, Adriana</creatorcontrib><title>Cardioprotection of ischaemic preconditioning is associated with inhibition of translocation of MLKL within the plasma membrane</title><title>Journal of cellular and molecular medicine</title><addtitle>J Cell Mol Med</addtitle><description>Necroptosis, a form of cell loss involving the RIP1‐RIP3‐MLKL axis, has been identified in cardiac pathologies while its inhibition is cardioprotective. We investigated whether the improvement of heart function because of ischaemic preconditioning is associated with mitigation of necroptotic signaling, and these effects were compared with a pharmacological antinecroptotic approach targeting RIP1. Langendorff‐perfused rat hearts were subjected to ischaemic preconditioning with or without a RIP1 inhibitor (Nec‐1s). Necroptotic signaling and the assessment of oxidative damage and a putative involvement of CaMKII in this process were analysed in whole tissue and subcellular fractions. Ischaemic preconditioning, Nec‐1s and their combination improved postischaemic heart function recovery and reduced infarct size to a similar degree what was in line with the prevention of MLKL oligomerization and translocation to the membrane. On the other hand, membrane peroxidation and apoptosis were unchanged by either approach. Ischaemic preconditioning failed to ameliorate ischaemia–reperfusion‐induced increase in RIP1 and RIP3 while pSer229‐RIP3 levels were reduced only by Nec‐1s. In spite of the additive phosphorylation of CaMKII and PLN because of ditherapy, the postischaemic contractile force and relaxation was comparably improved in all the intervention groups while antiarrhythmic effects were observed in the ischaemic preconditioning group only. Necroptosis inhibition seems to be involved in cardioprotection of ischaemic preconditioning and is comparable but not intensified by an anti‐RIP1 agent. Changes in oxidative stress nor CaMKII signaling are unlikely to explain the beneficial effects.</description><subject>Animals</subject><subject>Anti-Arrhythmia Agents - pharmacology</subject><subject>Apoptosis</subject><subject>Apoptosis - drug effects</subject><subject>Ca2+/calmodulin-dependent protein kinase II</subject><subject>Calcium-Binding Proteins - genetics</subject><subject>Calcium-Binding Proteins - metabolism</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics</subject><subject>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</subject><subject>Cell Membrane - drug effects</subject><subject>Cell Membrane - metabolism</subject><subject>Gene Expression Regulation</subject><subject>Heart</subject><subject>Heart - drug effects</subject><subject>Heart - physiopathology</subject><subject>Heart function</subject><subject>Imidazoles - pharmacology</subject><subject>Indoles - pharmacology</subject><subject>Inhibition</subject><subject>ischaemia‐reperfusion injury</subject><subject>Ischemia</subject><subject>Ischemic Preconditioning, Myocardial</subject><subject>Male</subject><subject>Muscle contraction</subject><subject>Myocardial Reperfusion Injury - genetics</subject><subject>Myocardial Reperfusion Injury - metabolism</subject><subject>Myocardial Reperfusion Injury - pathology</subject><subject>Myocardial Reperfusion Injury - therapy</subject><subject>Myocytes, Cardiac - drug effects</subject><subject>Myocytes, Cardiac - metabolism</subject><subject>Myocytes, Cardiac - pathology</subject><subject>Necroptosis</subject><subject>Necrosis - genetics</subject><subject>Necrosis - metabolism</subject><subject>Necrosis - pathology</subject><subject>Necrosis - prevention & control</subject><subject>Oligomerization</subject><subject>Organ Culture Techniques</subject><subject>Original</subject><subject>Oxidative Stress</subject><subject>Peroxidation</subject><subject>Phosphorylation</subject><subject>Phosphorylation - drug effects</subject><subject>Preconditioning</subject><subject>Protein Kinases - genetics</subject><subject>Protein Kinases - metabolism</subject><subject>Protein Serine-Threonine Kinases - antagonists & inhibitors</subject><subject>Protein Serine-Threonine Kinases - genetics</subject><subject>Protein Serine-Threonine Kinases - metabolism</subject><subject>Protein Transport - drug effects</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptor-Interacting Protein Serine-Threonine Kinases - genetics</subject><subject>Receptor-Interacting Protein Serine-Threonine Kinases - metabolism</subject><subject>Reperfusion</subject><subject>RIP1 inhibition</subject><subject>Signal Transduction</subject><subject>Translocation</subject><issn>1582-1838</issn><issn>1582-4934</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>24P</sourceid><sourceid>WIN</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>eNp9kU9vEzEQxS1ERUvgwgdAlrggpBT_390LUhVRoE3EBc6W15ntOlrbi72h6omvXqdJKuBQX2zN_Pw08x5Cbyg5p-V83FjvzylXTfUMnVFZs7louHh-eNOa16foZc4bQriivHmBTlnTMEoEO0N_FiatXRxTnMBOLgYcO-yy7Q14Z_GYwMawdruOCzelg03O0TozwRrfuqnHLvSudcevUzIhD9GaY2G1vF4-gC7gqQc8DiZ7gz34tqDwCp10Zsjw-nDP0M_Lzz8WX-fL71--LS6WcytEXc3bTkluOwkNp5VigihZW9VJSRi3Vtq66yrgQllVW8mrwoCUVWtBUSIpM3yGPu11x23rYW0hlEkHPSbnTbrT0Tj9bye4Xt_E31oVh-vi5wy9Pwik-GsLedK-2ATDUJaI26wZkZUQXDSkoO_-Qzdxm0JZr1CN4LJSkhXqw56yKeacoHschhK9y1XvctUPuRb47d_jP6LHIAtA98CtG-DuCSl9tVit9qL3W9ewIw</recordid><startdate>201809</startdate><enddate>201809</enddate><creator>Szobi, Adrián</creator><creator>Farkašová‐Ledvényiová, Veronika</creator><creator>Lichý, Martin</creator><creator>Muráriková, Martina</creator><creator>Čarnická, Slávka</creator><creator>Ravingerová, Tatiana</creator><creator>Adameová, Adriana</creator><general>John Wiley & Sons, Inc</general><general>John Wiley and Sons Inc</general><scope>24P</scope><scope>WIN</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>7QP</scope><scope>7TK</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>88I</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>CCPQU</scope><scope>DWQXO</scope><scope>FR3</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>M2P</scope><scope>M7P</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>Q9U</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0002-9803-043X</orcidid></search><sort><creationdate>201809</creationdate><title>Cardioprotection of ischaemic preconditioning is associated with inhibition of translocation of MLKL within the plasma membrane</title><author>Szobi, Adrián ; Farkašová‐Ledvényiová, Veronika ; Lichý, Martin ; Muráriková, Martina ; Čarnická, Slávka ; Ravingerová, Tatiana ; Adameová, Adriana</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4487-bf653cf5e93176240658c6f55023cc5c8ff7e346c68c537176e557bce610512a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Anti-Arrhythmia Agents - pharmacology</topic><topic>Apoptosis</topic><topic>Apoptosis - drug effects</topic><topic>Ca2+/calmodulin-dependent protein kinase II</topic><topic>Calcium-Binding Proteins - genetics</topic><topic>Calcium-Binding Proteins - metabolism</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics</topic><topic>Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism</topic><topic>Cell Membrane - drug effects</topic><topic>Cell Membrane - metabolism</topic><topic>Gene Expression Regulation</topic><topic>Heart</topic><topic>Heart - drug effects</topic><topic>Heart - physiopathology</topic><topic>Heart function</topic><topic>Imidazoles - pharmacology</topic><topic>Indoles - pharmacology</topic><topic>Inhibition</topic><topic>ischaemia‐reperfusion injury</topic><topic>Ischemia</topic><topic>Ischemic Preconditioning, Myocardial</topic><topic>Male</topic><topic>Muscle contraction</topic><topic>Myocardial Reperfusion Injury - genetics</topic><topic>Myocardial Reperfusion Injury - metabolism</topic><topic>Myocardial Reperfusion Injury - pathology</topic><topic>Myocardial Reperfusion Injury - therapy</topic><topic>Myocytes, Cardiac - drug effects</topic><topic>Myocytes, Cardiac - metabolism</topic><topic>Myocytes, Cardiac - pathology</topic><topic>Necroptosis</topic><topic>Necrosis - genetics</topic><topic>Necrosis - metabolism</topic><topic>Necrosis - pathology</topic><topic>Necrosis - prevention & control</topic><topic>Oligomerization</topic><topic>Organ Culture Techniques</topic><topic>Original</topic><topic>Oxidative Stress</topic><topic>Peroxidation</topic><topic>Phosphorylation</topic><topic>Phosphorylation - drug effects</topic><topic>Preconditioning</topic><topic>Protein Kinases - genetics</topic><topic>Protein Kinases - metabolism</topic><topic>Protein Serine-Threonine Kinases - antagonists & inhibitors</topic><topic>Protein Serine-Threonine Kinases - genetics</topic><topic>Protein Serine-Threonine Kinases - metabolism</topic><topic>Protein Transport - drug effects</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptor-Interacting Protein Serine-Threonine Kinases - genetics</topic><topic>Receptor-Interacting Protein Serine-Threonine Kinases - metabolism</topic><topic>Reperfusion</topic><topic>RIP1 inhibition</topic><topic>Signal Transduction</topic><topic>Translocation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Szobi, Adrián</creatorcontrib><creatorcontrib>Farkašová‐Ledvényiová, Veronika</creatorcontrib><creatorcontrib>Lichý, Martin</creatorcontrib><creatorcontrib>Muráriková, Martina</creatorcontrib><creatorcontrib>Čarnická, Slávka</creatorcontrib><creatorcontrib>Ravingerová, Tatiana</creatorcontrib><creatorcontrib>Adameová, Adriana</creatorcontrib><collection>Wiley Online Library (Open Access Collection)</collection><collection>Wiley Online Library (Open Access Collection)</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>Calcium & Calcified Tissue Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</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>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection (ProQuest)</collection><collection>ProQuest One Community College</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>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>Science Database (ProQuest)</collection><collection>Biological Science Database</collection><collection>Biotechnology and BioEngineering Abstracts</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>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Journal of cellular and molecular medicine</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Szobi, Adrián</au><au>Farkašová‐Ledvényiová, Veronika</au><au>Lichý, Martin</au><au>Muráriková, Martina</au><au>Čarnická, Slávka</au><au>Ravingerová, Tatiana</au><au>Adameová, Adriana</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cardioprotection of ischaemic preconditioning is associated with inhibition of translocation of MLKL within the plasma membrane</atitle><jtitle>Journal of cellular and molecular medicine</jtitle><addtitle>J Cell Mol Med</addtitle><date>2018-09</date><risdate>2018</risdate><volume>22</volume><issue>9</issue><spage>4183</spage><epage>4196</epage><pages>4183-4196</pages><issn>1582-1838</issn><eissn>1582-4934</eissn><abstract>Necroptosis, a form of cell loss involving the RIP1‐RIP3‐MLKL axis, has been identified in cardiac pathologies while its inhibition is cardioprotective. We investigated whether the improvement of heart function because of ischaemic preconditioning is associated with mitigation of necroptotic signaling, and these effects were compared with a pharmacological antinecroptotic approach targeting RIP1. Langendorff‐perfused rat hearts were subjected to ischaemic preconditioning with or without a RIP1 inhibitor (Nec‐1s). Necroptotic signaling and the assessment of oxidative damage and a putative involvement of CaMKII in this process were analysed in whole tissue and subcellular fractions. Ischaemic preconditioning, Nec‐1s and their combination improved postischaemic heart function recovery and reduced infarct size to a similar degree what was in line with the prevention of MLKL oligomerization and translocation to the membrane. On the other hand, membrane peroxidation and apoptosis were unchanged by either approach. Ischaemic preconditioning failed to ameliorate ischaemia–reperfusion‐induced increase in RIP1 and RIP3 while pSer229‐RIP3 levels were reduced only by Nec‐1s. In spite of the additive phosphorylation of CaMKII and PLN because of ditherapy, the postischaemic contractile force and relaxation was comparably improved in all the intervention groups while antiarrhythmic effects were observed in the ischaemic preconditioning group only. Necroptosis inhibition seems to be involved in cardioprotection of ischaemic preconditioning and is comparable but not intensified by an anti‐RIP1 agent. Changes in oxidative stress nor CaMKII signaling are unlikely to explain the beneficial effects.</abstract><cop>England</cop><pub>John Wiley & Sons, Inc</pub><pmid>29921042</pmid><doi>10.1111/jcmm.13697</doi><tpages>14</tpages><orcidid>https://orcid.org/0000-0002-9803-043X</orcidid><oa>free_for_read</oa></addata></record> |
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| ispartof | Journal of cellular and molecular medicine, 2018-09, Vol.22 (9), p.4183-4196 |
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| source | MEDLINE; DOAJ Directory of Open Access Journals; Access via Wiley Online Library; EZB-FREE-00999 freely available EZB journals; Wiley Online Library (Open Access Collection); PubMed Central |
| subjects | Animals Anti-Arrhythmia Agents - pharmacology Apoptosis Apoptosis - drug effects Ca2+/calmodulin-dependent protein kinase II Calcium-Binding Proteins - genetics Calcium-Binding Proteins - metabolism Calcium-Calmodulin-Dependent Protein Kinase Type 2 - genetics Calcium-Calmodulin-Dependent Protein Kinase Type 2 - metabolism Cell Membrane - drug effects Cell Membrane - metabolism Gene Expression Regulation Heart Heart - drug effects Heart - physiopathology Heart function Imidazoles - pharmacology Indoles - pharmacology Inhibition ischaemia‐reperfusion injury Ischemia Ischemic Preconditioning, Myocardial Male Muscle contraction Myocardial Reperfusion Injury - genetics Myocardial Reperfusion Injury - metabolism Myocardial Reperfusion Injury - pathology Myocardial Reperfusion Injury - therapy Myocytes, Cardiac - drug effects Myocytes, Cardiac - metabolism Myocytes, Cardiac - pathology Necroptosis Necrosis - genetics Necrosis - metabolism Necrosis - pathology Necrosis - prevention & control Oligomerization Organ Culture Techniques Original Oxidative Stress Peroxidation Phosphorylation Phosphorylation - drug effects Preconditioning Protein Kinases - genetics Protein Kinases - metabolism Protein Serine-Threonine Kinases - antagonists & inhibitors Protein Serine-Threonine Kinases - genetics Protein Serine-Threonine Kinases - metabolism Protein Transport - drug effects Rats Rats, Wistar Receptor-Interacting Protein Serine-Threonine Kinases - genetics Receptor-Interacting Protein Serine-Threonine Kinases - metabolism Reperfusion RIP1 inhibition Signal Transduction Translocation |
| title | Cardioprotection of ischaemic preconditioning is associated with inhibition of translocation of MLKL within the plasma membrane |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-13T13%3A51%3A12IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Cardioprotection%20of%20ischaemic%20preconditioning%20is%20associated%20with%20inhibition%20of%20translocation%20of%20MLKL%20within%20the%20plasma%20membrane&rft.jtitle=Journal%20of%20cellular%20and%20molecular%20medicine&rft.au=Szobi,%20Adri%C3%A1n&rft.date=2018-09&rft.volume=22&rft.issue=9&rft.spage=4183&rft.epage=4196&rft.pages=4183-4196&rft.issn=1582-1838&rft.eissn=1582-4934&rft_id=info:doi/10.1111/jcmm.13697&rft_dat=%3Cproquest_pubme%3E2057443490%3C/proquest_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2094357652&rft_id=info:pmid/29921042&rfr_iscdi=true |