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Vinnakota 2016b Biophys J

From Bioblast
Publications in the MiPMap
Vinnakota KC, Singhal A, Van den Bergh F, Bagher-Oskouei M, Wiseman RW, Beard DA (2016) Open-loop control of oxidative phosphorylation in skeletal and cardiac muscle mitochondria by Ca2+. Biophys J 110:954-61.

ยป PMID: 26910432

Vinnakota KC, Singhal A, Van den Bergh F, Bagher-Oskouei M, Wiseman RW, Beard DA (2016) Biophys J

Abstract: In cardiac muscle, mitochondrial ATP synthesis is driven by demand for ATP through feedback from the products of ATP hydrolysis. However, in skeletal muscle at higher workloads there is an apparent contribution of open-loop stimulation of ATP synthesis. Open-loop control is defined as modulation of flux through a biochemical pathway by a moiety, which is not a reactant or a product of the biochemical reactions in the pathway. The role of calcium, which is known to stimulate the activity of mitochondrial dehydrogenases, as an open-loop controller, was investigated in isolated cardiac and skeletal muscle mitochondria. The kinetics of NADH synthesis and respiration, feedback from ATP hydrolysis products, and stimulation by calcium were characterized in isolated mitochondria to test the hypothesis that calcium has a stimulatory role in skeletal muscle mitochondria not apparent in cardiac mitochondria. A range of respiratory states were obtained in cardiac and skeletal muscle mitochondria utilizing physiologically relevant concentrations of pyruvate and malate, and flux of respiration, NAD(P)H fluorescence, and rhodamine 123 fluorescence were measured over a range of extra mitochondrial calcium concentrations. We found that under these conditions calcium stimulates NADH synthesis in skeletal muscle mitochondria but not in cardiac mitochondria.

Copyright ยฉ 2016 Biophysical Society. Published by Elsevier Inc. All rights reserved.


โ€ข O2k-Network Lab: US MI Ann Arbor Beard DA


Labels: MiParea: Respiration 


Organism: Rat  Tissue;cell: Heart, Skeletal muscle  Preparation: Isolated mitochondria 

Regulation: Calcium  Coupling state: LEAK, OXPHOS  Pathway:HRR: Oxygraph-2k 

2016-03