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Cells 2018, 7(10), 175; https://doi.org/10.3390/cells7100175

Iron Depletion Affects Genes Encoding Mitochondrial Electron Transport Chain and Genes of Non­Oxidative Metabolism, Pyruvate Kinase and Lactate Dehydrogenase, in Primary Human Cardiac Myocytes Cultured upon Mechanical Stretch

1
Laboratory for Applied Research on Cardiovascular System, Department of Heart Diseases, Wroclaw Medical University, 50-367 Wroclaw, Poland
2
Department of Food Hygiene and Consumer Health Protection, Wroclaw University of Environmental and Life Sciences, 50-375 Wroclaw, Poland
3
Department of Heart Diseases, Wroclaw Medical University, 50-367 Wroclaw, Poland
4
Centre for Heart Diseases, Military Hospital, Wroclaw, Poland
*
Author to whom correspondence should be addressed.
Received: 24 September 2018 / Revised: 12 October 2018 / Accepted: 18 October 2018 / Published: 20 October 2018
(This article belongs to the Section Organelle Function)
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Abstract

(1) Background: Oxidative energy metabolism is presumed to rely on the optimal iron supply. Primary human cardiac myocytes (HCM) exposed to different iron availability conditions during mechanical stretch are anticipated to demonstrate expression changes of genes involved in aerobic and anaerobic metabolic pathways. (2) Methods: HCM were cultured for 48 h either in static conditions and upon mechanical stretch at the optimal versus reduced versus increased iron concentrations. We analyzed the expression of pyruvate kinase (PKM2), lactate dehydrogenase A (LDHA), and mitochondrial complexes I–V at the mRNA and protein levels. The concentration of l-lactate was assessed by means of lactate oxidase method-based kit. (3) Results: Reduced iron concentrations during mechanical work caused a decreased expression of complexes I–V (all p < 0.05). The expression of PKM2 and LDHA, as well as the medium concentration of l-lactate, was increased in these conditions (both p < 0.05). HCM exposed to the increased iron concentration during mechanical effort demonstrated a decreased expression of mitochondrial complexes (all p < 0.01); however, a decrement was smaller than in case of iron chelation (p < 0.05). The iron-enriched medium caused a decrease in expression of LDHA and did not influence the concentration of l-lactate. (4) Conclusions: During mechanical effort, the reduced iron availability enhances anaerobic glycolysis and extracellular lactate production, whilst decreasing mitochondrial aerobic pathway in HCM. Iron enrichment during mechanical effort may be protective in the context of intracellular protein machinery of non-oxidative metabolism with no effect on the extracellular lactate concentration. View Full-Text
Keywords: mitochondrial complexes; oxidative metabolism; non-oxidative metabolism; iron deficiency; iron excess; human cardiomyocytes mitochondrial complexes; oxidative metabolism; non-oxidative metabolism; iron deficiency; iron excess; human cardiomyocytes
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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Dziegala, M.; Kobak, K.A.; Kasztura, M.; Bania, J.; Josiak, K.; Banasiak, W.; Ponikowski, P.; Jankowska, E.A. Iron Depletion Affects Genes Encoding Mitochondrial Electron Transport Chain and Genes of Non­Oxidative Metabolism, Pyruvate Kinase and Lactate Dehydrogenase, in Primary Human Cardiac Myocytes Cultured upon Mechanical Stretch. Cells 2018, 7, 175.

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