Difference between revisions of "Liem 2008 Transl Res"
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|journal=Translation Research | |journal=Translation Research | ||
|abstract=We tested in the in vivo rat heart the hypothesis that although ischemic preconditioning can employ different signal transduction pathways, these pathways converge ultimately at the level of the mitochondrial respiratory chain. Infarct size produced by a 60-min coronary artery occlusion (69% ± 2% of the area at risk) was limited by a preceding 15-min coronary occlusion (48% ± 4%). Cardioprotection by this stimulus was triggered by adenosine receptor stimulation, which was followed by protein kinase C and tyrosine kinase activation and then mitochondrial K+ATP-channel opening. In contrast, cardioprotection by 3 cycles of 3-min coronary occlusions (infarct size 27% ± 5% of the area at risk) involved the release of reactive oxygen species, which was followed by protein kinase C and tyrosine kinase activation, but was independent of adenosine receptor stimulation and K+ATP-channel activation. However, both pathways decreased respiratory control index (RCI; state-3/state-2, using succinate as complex-II substrate) from 3.1 ± 0.2 in mitochondria from sham-treated hearts to 2.4 ± 0.2 and 2.5 ± 0.1 in hearts subjected to a single 15-min and triple 3-min coronary occlusions, respectively (both P < 0.05). The decreases in RCI were due to an increase in state-2 respiration, whereas state-3 respiration was unchanged. Abolition of cardioprotection by blockade of either signal transduction pathway was paralleled by a concomitant abolition of mitochondrial uncoupling. These observations are consistent with the concept that mild mitochondrial uncoupling contributes to infarct size limitation by various ischemic preconditioning stimuli, despite using different signal transduction pathways. In conclusion, in the in vivo rat heart, different ischemic preconditioning (IPC) stimuli can activate highly different signal transduction pathways, which seem to converge at the level of the mitochondria where they increase state-2 respiration. | |abstract=We tested in the in vivo rat heart the hypothesis that although ischemic preconditioning can employ different signal transduction pathways, these pathways converge ultimately at the level of the mitochondrial respiratory chain. Infarct size produced by a 60-min coronary artery occlusion (69% ± 2% of the area at risk) was limited by a preceding 15-min coronary occlusion (48% ± 4%). Cardioprotection by this stimulus was triggered by adenosine receptor stimulation, which was followed by protein kinase C and tyrosine kinase activation and then mitochondrial K<sup>+</sup><sub>ATP</sub>-channel opening. In contrast, cardioprotection by 3 cycles of 3-min coronary occlusions (infarct size 27% ± 5% of the area at risk) involved the release of reactive oxygen species, which was followed by protein kinase C and tyrosine kinase activation, but was independent of adenosine receptor stimulation and K+ATP-channel activation. However, both pathways decreased respiratory control index (RCI; state-3/state-2, using succinate as complex-II substrate) from 3.1 ± 0.2 in mitochondria from sham-treated hearts to 2.4 ± 0.2 and 2.5 ± 0.1 in hearts subjected to a single 15-min and triple 3-min coronary occlusions, respectively (both P < 0.05). The decreases in RCI were due to an increase in state-2 respiration, whereas state-3 respiration was unchanged. Abolition of cardioprotection by blockade of either signal transduction pathway was paralleled by a concomitant abolition of mitochondrial uncoupling. These observations are consistent with the concept that mild mitochondrial uncoupling contributes to infarct size limitation by various ischemic preconditioning stimuli, despite using different signal transduction pathways. In conclusion, in the in vivo rat heart, different ischemic preconditioning (IPC) stimuli can activate highly different signal transduction pathways, which seem to converge at the level of the mitochondria where they increase state-2 respiration. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/18061124 PMID: 18061124 ] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/18061124 PMID: 18061124 ] | ||
}} | }} | ||
Revision as of 17:32, 29 September 2010
| Liem D, Manintveld O, Schoonderwoerd K, McFalls E, Heinen A, Verdouw P, Sluiter W, Duncker D (2008) Ischemic preconditioning modulates mitochondrial respiration, irrespective of the employed signal transduction pathway. Translational Research 151: 17-26. |
Liem D, Manintveld O, Schoonderwoerd K, McFalls E, Heinen A, Verdouw P, Sluiter W, Duncker D (2008) Translation Research
Abstract: We tested in the in vivo rat heart the hypothesis that although ischemic preconditioning can employ different signal transduction pathways, these pathways converge ultimately at the level of the mitochondrial respiratory chain. Infarct size produced by a 60-min coronary artery occlusion (69% ± 2% of the area at risk) was limited by a preceding 15-min coronary occlusion (48% ± 4%). Cardioprotection by this stimulus was triggered by adenosine receptor stimulation, which was followed by protein kinase C and tyrosine kinase activation and then mitochondrial K+ATP-channel opening. In contrast, cardioprotection by 3 cycles of 3-min coronary occlusions (infarct size 27% ± 5% of the area at risk) involved the release of reactive oxygen species, which was followed by protein kinase C and tyrosine kinase activation, but was independent of adenosine receptor stimulation and K+ATP-channel activation. However, both pathways decreased respiratory control index (RCI; state-3/state-2, using succinate as complex-II substrate) from 3.1 ± 0.2 in mitochondria from sham-treated hearts to 2.4 ± 0.2 and 2.5 ± 0.1 in hearts subjected to a single 15-min and triple 3-min coronary occlusions, respectively (both P < 0.05). The decreases in RCI were due to an increase in state-2 respiration, whereas state-3 respiration was unchanged. Abolition of cardioprotection by blockade of either signal transduction pathway was paralleled by a concomitant abolition of mitochondrial uncoupling. These observations are consistent with the concept that mild mitochondrial uncoupling contributes to infarct size limitation by various ischemic preconditioning stimuli, despite using different signal transduction pathways. In conclusion, in the in vivo rat heart, different ischemic preconditioning (IPC) stimuli can activate highly different signal transduction pathways, which seem to converge at the level of the mitochondria where they increase state-2 respiration.
Labels:
Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property.
HRR: Oxygraph-2k
