Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP
Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide dela...
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E-Artikel |
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| Sprache: |
Englisch |
| Erschienen: |
2000 |
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| Umfang: |
7 |
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| Reproduktion: |
Springer Online Journal Archives 1860-2002 |
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| Übergeordnetes Werk: |
in: Basic research in cardiology - 1937, 95(2000) vom: März, Seite 243-249 |
| Übergeordnetes Werk: |
volume:95 ; year:2000 ; month:03 ; pages:243-249 ; extent:7 |
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NLEJ208635610 |
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| 245 | 1 | 0 | |a Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP |
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| 520 | |a Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. | ||
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(DE-627)NLEJ208635610 DE-627 ger DE-627 rakwb eng Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. Springer Online Journal Archives 1860-2002 Carroll, Richard oth Yellon, Derek M. oth in Basic research in cardiology 1937 95(2000) vom: März, Seite 243-249 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:95 year:2000 month:03 pages:243-249 extent:7 http://dx.doi.org/10.1007/s003950050187 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 95 2000 3 243-249 7 |
| spelling |
(DE-627)NLEJ208635610 DE-627 ger DE-627 rakwb eng Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. Springer Online Journal Archives 1860-2002 Carroll, Richard oth Yellon, Derek M. oth in Basic research in cardiology 1937 95(2000) vom: März, Seite 243-249 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:95 year:2000 month:03 pages:243-249 extent:7 http://dx.doi.org/10.1007/s003950050187 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 95 2000 3 243-249 7 |
| allfields_unstemmed |
(DE-627)NLEJ208635610 DE-627 ger DE-627 rakwb eng Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. Springer Online Journal Archives 1860-2002 Carroll, Richard oth Yellon, Derek M. oth in Basic research in cardiology 1937 95(2000) vom: März, Seite 243-249 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:95 year:2000 month:03 pages:243-249 extent:7 http://dx.doi.org/10.1007/s003950050187 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 95 2000 3 243-249 7 |
| allfieldsGer |
(DE-627)NLEJ208635610 DE-627 ger DE-627 rakwb eng Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. Springer Online Journal Archives 1860-2002 Carroll, Richard oth Yellon, Derek M. oth in Basic research in cardiology 1937 95(2000) vom: März, Seite 243-249 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:95 year:2000 month:03 pages:243-249 extent:7 http://dx.doi.org/10.1007/s003950050187 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 95 2000 3 243-249 7 |
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(DE-627)NLEJ208635610 DE-627 ger DE-627 rakwb eng Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP 2000 7 nicht spezifiziert zzz rdacontent nicht spezifiziert z rdamedia nicht spezifiziert zu rdacarrier Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. Springer Online Journal Archives 1860-2002 Carroll, Richard oth Yellon, Derek M. oth in Basic research in cardiology 1937 95(2000) vom: März, Seite 243-249 (DE-627)NLEJ188985204 (DE-600)1458470-0 1435-1803 nnns volume:95 year:2000 month:03 pages:243-249 extent:7 http://dx.doi.org/10.1007/s003950050187 GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE AR 95 2000 3 243-249 7 |
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delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38map kinase and mitochondrial katp |
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Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP |
| abstract |
Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. |
| abstractGer |
Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. |
| abstract_unstemmed |
Abstract Evidence of delayed preconditioning (PC) in man is limited. Adenosine is proposed as a trigger via action on the A1 receptor in many species and the mitochondrial KATP channel is a likely end effector. We examined the ability of a brief, simulated ischemic episode on day one to provide delayed cardioprotection against lethal, simulated ischemia on day two in a human cardiac cell line with reference to the role of adenosine, the p38MAP kinase signalling pathway and mitochondrial KATP channel. Results: PC and adenosine administered on day 1 protected against cell death on day 2 as measured by LDH release and propidium iodide (PI) exclusion: (%LDH release: PC: 12.1 ± 1.1%, ADO: 11.9 ± 2.0% vs control: 36.4 ± 1.1%, %PI positive: PC: 14.6% ± 1.4%, ADO: 17.9 ± 2.0% vs control: 34.4 ± 2.0% respectively). This protection is abolished by treatment with SB203580 prior to the protective stimulus on day 1: [PC + SB (%LDH release 28.6 ± 2.8%, %PI positive 34.7 ± 2.2%) and ADO + SB (%LDH release 25.3 ± 2.9%; %PI positive 33.7 ± 7.3%)]. Similarly 5-hydroxydecanoate abolished protection, when given immediately prior to lethal simulated ischemia on day 2: [PC + 5-HD; (%LDH release 31.9 ± 4.8%; %PI positive 29.5 ± 2.0%) and ADO + 5-HD (%LDH release 36.9 ± 4.0%; %PI positive 34.8 ± 2%)]. Conclusion: In this model delayed PC can be mimicked by adenosine and involves the p38MAP kinase pathway and the mitochondrial KATP channel. |
| collection_details |
GBV_USEFLAG_U ZDB-1-SOJ GBV_NL_ARTICLE |
| title_short |
Delayed cardioprotection in a human cardiomyocyte-derived cell line: the role of adenosine, p38MAP kinase and mitochondrial KATP |
| url |
http://dx.doi.org/10.1007/s003950050187 |
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Carroll, Richard Yellon, Derek M. |
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| up_date |
2024-07-05T21:46:01.155Z |
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7.3998413 |