Heidler 2013 Abstract MiP2013
|Heidler J, Wittig I, Henze D, Krüger C, Kostin S, Braun T, Szibor M (2013) Functional plasticity of interfibrillary mitochondria as cardiac response mechanism to stress. Mitochondr Physiol Network 18.08.|
MiP2013, Book of Abstracts Open Access
Heidler J, Wittig I, Henze D, Krueger C, Kostin S, Braun T, Szibor M (2013)
A morphological hallmark of the failing human heart is a devastative autophagic degradation of cellular structures starting from the perinuclear region, proposed to actively shift the heart into a decompensated state . We studied heart samples from different species, i.e. a mouse model of cardiac specific expression of MCP1 that autonomously develops heart failure , hibernating Syrian hamsters  and a pig model of mitochondrial dysfunction exposed to hyperbaric oxygen.
Our data reveal an age-dependent increase of perinuclear degradation in mouse hearts that occurred prior to the onset of cardiac dysfunction. These center core-like lesions in the myofibrillar compartment are most likely the end-stage result of a vicious cycle that starts with a physiological response to lowered levels of cardiac workload. Accordingly we found that in hibernating Syrian hamsters under conditions of depressed metabolism interfibrillar mitochondria are reversibly silenced whilst subsarcolemmal mitochondria remain more active. Central remodeling of cardiomyocyte compartments is a phenomenon primarily known in the hibernating myocardium . Here we show in pig hearts that the isolated impairment of the interfibrillary compartment can be fully re-activated upon treatment with hyperbaric oxygen.
We conclude that differential compartment regulation by switching the activity status of mitochondrial sub-populations from on to off and vice versa might provide a hitherto unnoticed flexible on-demand plasticity in cardiomyocytes. Such alterations make proper myofibril contraction in the silenced compartment unlikely. Silenced mitochondria can be re-activated on demand. Only long-lasting mitochondrial silencing, e.g. upon chronic cardiac overload, might increase the risk of adverse cardiomyocyte remodeling.
• Keywords: interfibrillar mitochondria, subsarcolemmal mitochondria, metabolic suppression, Injuries and adaptation:Others, CV
• O2k-Network Lab: FI Helsinki Jacobs HT, DE Frankfurt Droese S
Labels: MiParea: Comparative MiP;environmental MiP Pathology: Other
Organism: Human, Mouse, Other mammals, Pig Tissue;cell: Heart Preparation: Intact organ, Homogenate, Isolated mitochondria Enzyme: Marker enzyme, Supercomplex Regulation: ATP production, Oxygen kinetics
1 - Dept of Molecular Hematology, Goethe University, Frankfurt, Germany;
2 - Functional Prote-omics, SFB 815 core unit, Faculty of Medicine, Goethe University, Frankfurt, Germany;
3 - Dr. Henze & Partner PartG, Praxis für Anästhesiologie, Halle a. d. Saale, Germany;
4 - Medical Af-fairs, Fa. cellpharm GmbH, Bad Vilbel, Germany;
5 - Dept I - Cardiac Development and Remodeling, Max Planck Institute for Heart and Lung Research, Bad Nauheim, Germany;
6 - Research Program of Molecular Neurology, University of Helsinki, Finland.
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