Heidler 2013 Abstract MiP2013

Heidler J, Wittig I, Henze D, Krüger C, Kostin S, Braun T, Szibor M (2013) Functional plasticity of interfibrillary mitochondria (IFM) as cardiac response mechanism to stress. Mitochondr Physiol Network 18.08.

Link:

MiP2013, Book of Abstracts Open Access

Heidler J, Wittig I, Henze D, Krueger C, Kostin S, Braun T, Szibor M (2013)

Event: MiP2013 Programme

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 [1]. We studied heart samples from different species, i.e. a mouse model of cardiac specific expression of MCP1 that autonomously develops heart failure [2], hibernating Syrian hamsters [3] 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 [4]. 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

Labels: MiParea: Comparative MiP;environmental MiP  Pathology: Other 

Organism: Human, Pig, Mouse, Other mammals  Tissue;cell: Heart  Preparation: Intact Organ"Intact Organ" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property., Homogenate, Isolated Mitochondria"Isolated Mitochondria" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property.  Enzyme: Marker Enzyme"Marker Enzyme" is not in the list (Adenine nucleotide translocase, Complex I, Complex II;succinate dehydrogenase, Complex III, Complex IV;cytochrome c oxidase, Complex V;ATP synthase, Inner mt-membrane transporter, Marker enzyme, Supercomplex, TCA cycle and matrix dehydrogenases, ...) of allowed values for the "Enzyme" property., Supercomplex  Regulation: ATP production, O2"O2" 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. 

MiP2013 

Affiliations and author contributions

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.

Email: heidler@em.uni-frankfurt.de

References

1. Hein S, Arnon E, Kostin S, Schönburg M, Elsässer A, Polyakova V, Bauer EP, Klövekorn W-P, Schaper J (2003) Pro-gression from compensated hypertrophy to failure in the pressure-overloaded human heart: structural deterioration and compensatory mechanisms. Circulation 107: 984–991.
2. Kolattukudy PE, Quach T, Bergese S, Breckenridge S, Hensley J, Altschuld R, Gordillo G, Klenotic S, Orosz C, Parker-Thornburg J (1998) Myocarditis induced by targeted expression of the MCP-1 gene in murine cardiac muscle. Am J Pathol 152: 101–111.
3.  Toole L, Belai A, Shochina M, Burnstock G (1999) The effects of hibernation on the myenteric plexus of the golden hamster small and large intestine. Cell Tissue Res 296: 479–487.
4.  Borgers M, Ausma J (1995) Structural aspects of the chronic hibernating myocardium in man. Basic Res Cardiol 90: 44–46.