Difference between revisions of "Borutaite 2015 Abstract MiPschool Cape Town 2015"
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{{Abstract | {{Abstract | ||
|title=Mitochondria and regulation of cell death during ischemia. | |||
|authors=Borutaite V | |||
|year=2015 | |year=2015 | ||
|event=MiPschool Cape Town 2015 | |event=MiPschool Cape Town 2015 | ||
|abstract=Opening of mitochondrial permeability transition pore (MPTP) is | |||
considered as one of the main determinants in ischemia-reperfusion induced | |||
myocardial injury. The involvement of MPTP in brain ischemia induced | |||
damage is less clear. MPTP causes permeabilization of | |||
mitochondrial membranes leading to the release of cytochrome c | |||
from mitochondria, mitochondrial dysfunction, caspase activation and | |||
apoptotic or necrotic death of cardiac or neuronal cells depending on | |||
cellular resources of ATP. In recent years various strategies aiming at | |||
pharmacological inhibition of MPTP during ischemia or reperfusion | |||
have been proposed, though the molecular mechanisms of regulation | |||
of MPTP are still unclear. The molecular composition of MPTP is also | |||
unresolved question. We have recently shown that low levels of NO may | |||
activate signalling pathways in cardiac and neuronal cells that involve | |||
protein kinases C and G which, in turn, may increase resistance of | |||
mitochondria to Ca<sup>2+</sup>- and ischemia-induced opening of MPTP. Analysis | |||
of phosphoproteome of mitochondria isolated from hearts treated with | |||
NO revealed several mitochondrial proteins, phosphorylation of which is | |||
affected by this treatment and which may be involved in MPTP formation. | |||
In this lecture, we will discuss current knowledge on structure of MPTP, | |||
experimental approaches to investigate MPTP functions and possible | |||
role of MPTP in ischemic heart and brain damage. | |||
|mipnetlab=LT Kaunas Borutaite V | |||
}} | }} | ||
{{Labeling}} | {{Labeling | ||
|organism=Human | |||
|tissues=Heart | |||
|preparations=Isolated mitochondria | |||
|injuries=Ischemia-reperfusion;preservation | |||
}} | |||
== Affiliations == | |||
Inst Neurosc, Lithuanian Univ Health Sc, Kaunas, Lithuania. - [email protected] | |||
Revision as of 16:22, 20 March 2015
| Mitochondria and regulation of cell death during ischemia. |
Link:
Borutaite V (2015)
Event: MiPschool Cape Town 2015
Opening of mitochondrial permeability transition pore (MPTP) is considered as one of the main determinants in ischemia-reperfusion induced myocardial injury. The involvement of MPTP in brain ischemia induced damage is less clear. MPTP causes permeabilization of mitochondrial membranes leading to the release of cytochrome c from mitochondria, mitochondrial dysfunction, caspase activation and apoptotic or necrotic death of cardiac or neuronal cells depending on cellular resources of ATP. In recent years various strategies aiming at pharmacological inhibition of MPTP during ischemia or reperfusion have been proposed, though the molecular mechanisms of regulation of MPTP are still unclear. The molecular composition of MPTP is also unresolved question. We have recently shown that low levels of NO may activate signalling pathways in cardiac and neuronal cells that involve protein kinases C and G which, in turn, may increase resistance of mitochondria to Ca2+- and ischemia-induced opening of MPTP. Analysis of phosphoproteome of mitochondria isolated from hearts treated with NO revealed several mitochondrial proteins, phosphorylation of which is affected by this treatment and which may be involved in MPTP formation. In this lecture, we will discuss current knowledge on structure of MPTP, experimental approaches to investigate MPTP functions and possible role of MPTP in ischemic heart and brain damage.
• O2k-Network Lab: LT Kaunas Borutaite V
Labels:
Stress:Ischemia-reperfusion;preservation"Ischemia-reperfusion;preservation" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Heart Preparation: Isolated mitochondria
Affiliations
Inst Neurosc, Lithuanian Univ Health Sc, Kaunas, Lithuania. - [email protected]
