Papadimitriou 2019 Sci Rep: Difference between revisions
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|abstract=Research in ฮฑ-actinin-3 knockout mice suggests a novel role for ฮฑ-actinin-3 as a mediator of cell signalling. We took advantage of naturally-occurring human "knockouts" (lacking ฮฑ-actinin-3 protein) to investigate the consequences of ฮฑ-actinin-3 deficiency on exercise-induced changes in mitochondrial-related genes and proteins, as well as endurance training adaptations. At baseline, we observed a compensatory increase of ฮฑ-actinin-2 protein in ACTN3 XX (ฮฑ-actinin-3 deficient; nโ=โ18) vs ACTN3 RR (expressing ฮฑ-actinin-3; nโ=โ19) participants but no differences between genotypes for markers of aerobic fitness or mitochondrial content and function. There was a main effect of genotype, without an interaction, for RCAN1-4 protein content (a marker of calcineurin activity). However, there was no effect of genotype on exercise-induced expression of genes associated with mitochondrial biogenesis, nor post-training physiological changes. In contrast to results in mice, loss of ฮฑ-actinin-3 is not associated with higher baseline endurance-related phenotypes, or greater adaptations to endurance exercise training in humans. | |abstract=Research in ฮฑ-actinin-3 knockout mice suggests a novel role for ฮฑ-actinin-3 as a mediator of cell signalling. We took advantage of naturally-occurring human "knockouts" (lacking ฮฑ-actinin-3 protein) to investigate the consequences of ฮฑ-actinin-3 deficiency on exercise-induced changes in mitochondrial-related genes and proteins, as well as endurance training adaptations. At baseline, we observed a compensatory increase of ฮฑ-actinin-2 protein in ACTN3 XX (ฮฑ-actinin-3 deficient; nโ=โ18) vs ACTN3 RR (expressing ฮฑ-actinin-3; nโ=โ19) participants but no differences between genotypes for markers of aerobic fitness or mitochondrial content and function. There was a main effect of genotype, without an interaction, for RCAN1-4 protein content (a marker of calcineurin activity). However, there was no effect of genotype on exercise-induced expression of genes associated with mitochondrial biogenesis, nor post-training physiological changes. In contrast to results in mice, loss of ฮฑ-actinin-3 is not associated with higher baseline endurance-related phenotypes, or greater adaptations to endurance exercise training in humans. | ||
|editor=[[Plangger M]], | |editor=[[Plangger M]], | ||
|mipnetlab=AU Melbourne Stepto NK | |||
}} | }} | ||
{{Labeling | {{Labeling | ||
|area=Respiration | |area=Respiration, Genetic knockout;overexpression, Exercise physiology;nutrition;life style | ||
|organism=Human | |||
|tissues=Skeletal muscle | |||
|couplingstates=LEAK, OXPHOS, ET | |||
|pathways=N, S, NS, ROX | |||
|instruments=Oxygraph-2k | |instruments=Oxygraph-2k | ||
|additional=Labels, 2019-09, | |additional=Labels, 2019-09, | ||
}} | }} | ||
Revision as of 15:18, 9 September 2019
| Papadimitriou ID, Eynon N, Yan X, Munson F, Jacques M, Kuang J, Voisin S, North KN, Bishop DJ (2019) A "human knockout" model to investigate the influence of the ฮฑ-actinin-3 protein on exercise-induced mitochondrial adaptations. Sci Rep 9:12688. |
Papadimitriou ID, Eynon N, Yan X, Munson F, Jacques M, Kuang J, Voisin S, North KN, Bishop DJ (2019) Sci Rep
Abstract: Research in ฮฑ-actinin-3 knockout mice suggests a novel role for ฮฑ-actinin-3 as a mediator of cell signalling. We took advantage of naturally-occurring human "knockouts" (lacking ฮฑ-actinin-3 protein) to investigate the consequences of ฮฑ-actinin-3 deficiency on exercise-induced changes in mitochondrial-related genes and proteins, as well as endurance training adaptations. At baseline, we observed a compensatory increase of ฮฑ-actinin-2 protein in ACTN3 XX (ฮฑ-actinin-3 deficient; nโ=โ18) vs ACTN3 RR (expressing ฮฑ-actinin-3; nโ=โ19) participants but no differences between genotypes for markers of aerobic fitness or mitochondrial content and function. There was a main effect of genotype, without an interaction, for RCAN1-4 protein content (a marker of calcineurin activity). However, there was no effect of genotype on exercise-induced expression of genes associated with mitochondrial biogenesis, nor post-training physiological changes. In contrast to results in mice, loss of ฮฑ-actinin-3 is not associated with higher baseline endurance-related phenotypes, or greater adaptations to endurance exercise training in humans.
โข Bioblast editor: Plangger M โข O2k-Network Lab: AU Melbourne Stepto NK
Labels: MiParea: Respiration, Genetic knockout;overexpression, Exercise physiology;nutrition;life style
Organism: Human
Tissue;cell: Skeletal muscle
Coupling state: LEAK, OXPHOS, ET Pathway: N, S, NS, ROX HRR: Oxygraph-2k
Labels, 2019-09
