Age influences DNA methylation and gene expression of COX7A1 in human skeletal muscle.
Open accessAbstract
Aims/hypothesis Reduced oxidative capacity of the mitochondria in skeletal muscle has been suggested to contribute to insulin resistance and type 2 diabetes. Moreover, a set of genes influencing oxidative phosphorylation (OXPHOS) is downregulated in diabetic muscle. Here we studied whether genetic, epigenetic and non-genetic factors influence a component of the respiratory chain, COX7A1, previously shown to be downregulated in skeletal muscle from patients with type 2 diabetes. The specific aims were to: (1) evaluate the impact of genetic (single nucleotide polymorphisms [SNPs]), epigenetic (DNA methylation) and non-genetic (age) factors on the expression of COX7A1 in human skeletal muscle; and (2) investigate whether common variants in the COX7A1 gene are associated with increased risk of type 2 diabetes.Methods COX7A1 mRNA expression was analysed in muscle biopsies from young (n = 110) and elderly (n = 86) non-diabetic twins and related to measures of in vivo metabolism. Genetic variants (three SNPs) from the COX7A1 locus were genotyped in the twins and in two independent type 2 diabetes case-control cohorts (n = 1466 and 6380, respectively). DNA methylation of the COX7A1 promoter was analysed in a subset of twins (ten young, ten elderly) using bisulphite sequencing.Results While DNA methylation of the COX7A1 promoter was increased in muscle from elderly compared with young twins (19.9 +/- 8.3% vs 1.8 +/- 2.7%; p = 0.035), the opposite was found for COX7A1 mRNA expression (elderly 1.00 +/- 0.05 vs young 1.68 +/- 0.06; p = 0.0005). The heritability of COX7A1 expression was estimated to be 50% in young and 72% in elderly twins. One of the polymorphisms investigated, rs753420, influenced basal COX7A1 expression in muscle of young (p = 0.0001) but not of elderly twins. The transcript level of COX7A1 was associated with increased in vivo glucose uptake and VO(2max) (p = 0.009 and p = 0.001, respectively). We did not observe any genetic association between COX7A1 polymorphisms and type 2 diabetes after correcting for multiple testing.Conclusions/interpretation Our results provide further evidence for age as a factor influencing DNA methylation and expression of OXPHOS genes, and thereby in vivo metabolism.
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Epigenetic mechanisms may also contribute to these patterns because reduced expression parallels increased DNA methylation of both the COX7A1 promoter and NDUFB6.
“Interestingly, epigenetic mechanisms may also contribute to these patterns because reduced expression parallels increased DNA methylation of both the COX7A1 promoter (136) and NDUFB6 (137, 139).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [136]
Expression of COX7A1, a complex IV gene down-regulated in type 2 DM, is heritable (50-72% heritability, as assessed by analysis in monozygotic and dizygotic twins), indicating a strong genetic or shared familial environmental contribution.
“For example, expression of COX7A1, a complex IV gene down-regulated in type 2 DM, is heritable (50 -72% heritability, as assessed by analysis in monozygotic and dizygotic twins), indicating a strong genetic or shared familial environmental contribution (136).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [136]
Aging is linked to impaired oxidative function in parallel with reductions in OXPHOS gene expression, including COX7A1, NDUFB6, and ATP50.
“Aging is also linked to impaired oxidative function (140) in parallel with reductions in OXPHOS gene expression, including COX7A1, NDUFB6, and ATP50 (136 -138).”
From The role of mitochondria in the pathogenesis of type 2 diabetes (2010) · cites this paper as [136]
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- Authors
- Rönn, T., Poulsen, P., Hansson, O., Holmkvist, J., Almgren, P., Nilsson, P., Tuomi, T., Isomaa, B., Groop, L., Vaag, A., & Ling, C.
- Affiliations
- Lund University (SE)
- University of Helsinki (FI)
- Corresponding author
- Ling, C.
- Venue
- Diabetologia
- Published
- 2008-05-17
- Volume
- 51
- Issue
- 7
- Pages
- 1159-1168
- ISSN
- 0012-186X (ISSN-L)
- 1432-0428
- OpenAlex
- W2077687426
- Cited by
- 175
- References
- 51
- Citations by year
- 2026: 3 · 2025: 4 · 2024: 2 · 2023: 7 · 2022: 8 · 2021: 7 · 2020: 10 · 2019: 10 · 2018: 6 · 2017: 11 · 2016: 11 · 2015: 17 · 2014: 12 · 2013: 7 · 2012: 15
- FWCI
- 6.15
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Diabetologia (publishedVersion)
- PubMed (publishedVersion)
- Lund University Publications (Lund University) (submittedVersion)
- Research at the University of Copenhagen (University of Copenhagen) (submittedVersion)
- Funders
- Sundhed og Sygdom, Det Frie Forskningsråd
- Lunds Universitet
- Novo Nordisk
- Vetenskapsrådet
- Malmö Högskola
- Region Skåne
- Diabetesforeningen
- Medical Research Council
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Epigenetics and DNA Methylation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
- Keywords
- COX7A1, DNA methylation, gene expression, skeletal muscle, aging, type 2 diabetes, oxidative phosphorylation, electron transport chain, single nucleotide polymorphisms, promoter methylation, heritability, glucose uptake, VO2max, mitochondrial oxidative capacity, insulin resistance, twins, genetic susceptibility, epigenetics, gene-environment interaction
- MeSH terms
- Adult, Aged, Aging, Biopsy, Electron Transport Complex IV, Diabetes Mellitus, Type 2, Female, Gene Expression Regulation, Humans, Insulin Resistance, Male, Middle Aged, Oxidative Phosphorylation, Promoter Regions, Genetic, Risk Factors, RNA, Messenger, Muscle, Skeletal, DNA Methylation, Genetic Predisposition to Disease, Polymorphism, Single Nucleotide, Epigenesis, Genetic
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