Edit Abstract: Wuest 2017 Abstract MITOEAGLE Barcelona

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Abstract:	[[Image:MITOEAGLE-logo.jpg\|left\|100px\|link=http://www.mitoglobal.org/index.php/MITOEAGLE\|COST Action MITOEAGLE]] In cardiac hypertrophy (CH) and heart failure (HF), alterations occur in mitochondrial enzyme content and activities but the origin and implications of these changes for mitochondrial function need to be resolved. Right ventricular CH or HF was induced by monocrotaline injection, which causes pulmonary artery hypertension, in rats. Results were compared with saline injection (CON). NAD(P)H and FAD autofluorescence were recorded in thin intact cardiac trabeculae during transitions in stimulation frequency, to assess mitochondrial Complex I and Complex II function, respectively. Mitochondrial oxygen consumption, morphology, protein content, and enzymatic activity were assessed. NAD(P)H autofluorescence upon an increase in stimulation frequency showed a rapid decline followed by a slow recovery. The amplitude of the early rapid change in NAD(P)H autofluorescence was severely depressed in CH and HF compared with CON, but to a lesser extent for FAD in CH and HF. Complex I-coupled respiration showed a ∼3.5-fold reduction in CH and HF; Complex II-coupled respiration was depressed two-fold in HF. Protein content of Complex I subunits and isolated Complex I activity in supercomplexes were modestly reduced in CH and HF. Mitochondrial volume density was similar, but remodeling was evident from changes in ultrastructure and fusion/fission indices in CH and HF [1]. Complex I dysfunction is observed in CH and HF, although it remains to be determined whether this is a cause or consequence of mitochondrial remodeling. Future work is directed to identify compounds that alter mitochondrial bio-energetic function in cardiac myocytes, using Oroboros Oxygraph-2k and Seahorse XF technology.
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MiP areas:	Respiration Instruments;methods mt-Biogenesis;mt-density mt-Structure;fission;fusion mt-Membrane mtDNA;mt-genetics nDNA;cell genetics Genetic knockout;overexpression Comparative MiP;environmental MiP Gender Developmental biology Exercise physiology;nutrition;life style mt-Medicine Patients Pharmacology;toxicology mt-Awareness
Pathological states:	Aging;senescence Alzheimer's Autism Cancer Cardiovascular COPD Diabetes Inherited Infectious Myopathy Neurodegenerative Obesity Parkinson's Sepsis Other
Stress conditions:	Cell death Cryopreservation Ischemia-reperfusion Permeability transition Oxidative stress;RONS Temperature Hypoxia Mitochondrial disease
Organism:	Human Pig Mouse Rat Guinea pig Bovines Horse Dog Rabbit Cat Other mammals Chicken Zebrafish Drosophila Artemia Caenorhabditis elegans Saccharomyces cerevisiae Birds Reptiles Amphibians Fishes Chelicerates Crustaceans Hexapods Myriapods Annelids Molluscs Nematodes Other invertebrates Fungi Plants Protists Eubacteria Archea
Tissues;cells:	Heart Skeletal muscle Nervous system Liver Kidney Lung;gill Islet cell;pancreas;thymus Endothelial;epithelial;mesothelial cell Blood cells Fat Genital Other cell lines CHO HEK HeLa Neuroblastoma Fibroblast HUVEC Macrophage-derived Lymphocyte Platelet Stem cells
Preparations:	Intact organism Intact organ Permeabilized cells Permeabilized tissue Homogenate Isolated mitochondria SMP Chloroplasts Enzyme Oxidase;biochemical oxidation Intact cells
Enzymes:	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 Uncoupling protein
Regulation:	Aerobic glycolysis ADP ATP ATP production AMP Calcium Coupling efficiency;uncoupling Cyt c Flux control Inhibitor Ion;substrate transport mt-Membrane potential Oxygen kinetics PCr;Cr pH Phosphate Redox state Substrate Temperature Threshold;excess capacity Uncoupler Fatty acid Amino acid Q-junction effect
Coupling:	LEAK ROUTINE OXPHOS ET
Pathways:	F N S Gp DQ CIV NS Other combinations ROX
High-resolution respirometry:	Oxygraph-2k TIP2k O2k-Fluorometer pH NO TPP Ca O2k-Spectrophotometer O2k-Manual O2k-Protocol Theory NextGen-O2k
Event:	A1 A2 A3 A4 B1 B2 B3 B4 C1 C2 C3 C4 D1 D2 D3 D4 E1 E2 Oral Poster P-flash Review
Additional labels:	(separate values by colon)

Free text: Any additional information (e.g. affiliations of authors). == Affiliation == :::: Lab Genetic Metabolic Diseases, Academic Medical Center, Amsterdam, The Netherlands. – r.wust@amc.uva.nl == References == :::# Wuest RCI, de Vries HJ, Wintjes LT, Rodenburg RJ, Niessen HW, Stienen GJ (2016) Mitochondrial Complex I dysfunction and altered NAD(P)H kinetics in rat myocardium in cardiac right ventricular hypertrophy and failure. Cardiovasc Res 111:362-72.

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Edit Abstract: Wuest 2017 Abstract MITOEAGLE Barcelona

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