Carbon monoxide shifts energetic metabolism from glycolysis to oxidative phosphorylation in endothelial cells

Carbon monoxide (CO) modulates mitochondrial respiration, but the mechanisms involved are not completely understood. The aim of the present study was to investigate the acute effects of CO on bioenergetics and metabolism in intact EA.hy926 endothelial cells using live cell imaging techniques. Our fi...

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Bibliographic Details
Published in:FEBS letters 2016-10, Vol.590 (20), p.3469-3480
Main Authors: Kaczara, Patrycja, Motterlini, Roberto, Kus, Kamil, Zakrzewska, Agnieszka, Abramov, Andrey Y., Chlopicki, Stefan
Format: Article
Language:English
Subjects:
Adenosine Triphosphate - metabolism
Calcium - metabolism
carbon monoxide
Carbon Monoxide - metabolism
Cell Line
CO‐releasing molecule
Electron Transport Complex I - drug effects
Electron Transport Complex II - drug effects
Endothelial Cells - metabolism
endothelium
Energy Metabolism - drug effects
glycolysis
Glycolysis - drug effects
Humans
Manganese - chemistry
Membrane Potential, Mitochondrial - drug effects
Mitochondria - metabolism
Organometallic Compounds - chemistry
Organometallic Compounds - pharmacology
Oxidative Phosphorylation
respiration
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Summary:Carbon monoxide (CO) modulates mitochondrial respiration, but the mechanisms involved are not completely understood. The aim of the present study was to investigate the acute effects of CO on bioenergetics and metabolism in intact EA.hy926 endothelial cells using live cell imaging techniques. Our findings indicate that CORM‐401, a compound that liberates CO, reduces ATP production from glycolysis, and induces a mild mitochondrial depolarization. In addition, CO from CORM‐401 increases mitochondrial calcium and activates complexes I and II. The subsequent increase in mitochondrial respiration leads to ATP production through oxidative phosphorylation. Thus, our results show that nonactivated endothelial cells rely primarily on glycolysis, but in the presence of CO, mitochondrial Ca2+ increases and activates respiration that shifts the metabolism of endothelial cells from glycolysis‐ to oxidative phosphorylation‐dependent ATP production.
ISSN:0014-5793
1873-3468
DOI:10.1002/1873-3468.12434