Genome‐wide DNA methylation changes with age in disease‐free human skeletal muscle

Summary A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome‐wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging....

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Published inAging cell Vol. 13; no. 2; pp. 360 - 366
Main Authors Zykovich, Artem, Hubbard, Alan, Flynn, James M., Tarnopolsky, Mark, Fraga, Mario F., Kerksick, Chad, Ogborn, Dan, MacNeil, Lauren, Mooney, Sean D., Melov, Simon
Format Journal Article
LanguageEnglish
Published England John Wiley & Sons, Inc 01.04.2014
BlackWell Publishing Ltd
Subjects
Adolescent
Adult
Aged
Aging - genetics
Base Composition - genetics
CpG Islands
DNA methylation
DNA Methylation - genetics
epigenome
Gene Expression Regulation
Gene Ontology
Genome, Human - genetics
genomics
human aging
Humans
Male
Muscle, Skeletal - metabolism
Original
postmitotic
Signal Transduction - genetics
skeletal muscle
Young Adult
postmitotic
DNA methylation
genomics
epigenome
skeletal muscle
human aging
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Abstract Summary A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome‐wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3′ end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
AbstractList Summary A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome-wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3' end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome‐wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3′ end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
Summary A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome‐wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3′ end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome-wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3' end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome-wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3' end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome-wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3′ end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the first time a genome-wide study of DNA methylation dynamics in skeletal muscle of healthy male individuals during normal human aging. We predominantly observed hypermethylation throughout the genome within the aged group as compared to the young subjects. Differentially methylated CpG (dmCpG) nucleotides tend to arise intragenically and are underrepresented in promoters and are overrepresented in the middle and 3' end of genes. The intragenic methylation changes are overrepresented in genes that guide the formation of the junction of the motor neuron and myofibers. We report a low level of correlation of gene expression from previous studies of aged muscle with our current analysis of DNA methylation status. For those genes that had both changes in methylation and gene expression with age, we observed a reverse correlation, with the exception of intragenic hypermethylated genes that were correlated with an increased gene expression. We suggest that a minimal number of dmCpG sites or select sites are required to be altered in order to correlate with gene expression changes. Finally, we identified 500 dmCpG sites that perform well in discriminating young from old samples. Our findings highlight epigenetic links between aging postmitotic skeletal muscle and DNA methylation.
Author Tarnopolsky, Mark
Mooney, Sean D.
Fraga, Mario F.
Ogborn, Dan
Flynn, James M.
Kerksick, Chad
Melov, Simon
Hubbard, Alan
MacNeil, Lauren
Zykovich, Artem
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  organization: Buck Institute for Research on Aging
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  surname: Hubbard
  fullname: Hubbard, Alan
  organization: University of California
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  givenname: James M.
  surname: Flynn
  fullname: Flynn, James M.
  organization: Buck Institute for Research on Aging
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  givenname: Mark
  surname: Tarnopolsky
  fullname: Tarnopolsky, Mark
  organization: McMaster University Medical Center
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  givenname: Mario F.
  surname: Fraga
  fullname: Fraga, Mario F.
  organization: Universidad de Oviedo
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  givenname: Chad
  surname: Kerksick
  fullname: Kerksick, Chad
  organization: University of New Mexico
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  organization: Buck Institute for Research on Aging
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  givenname: Simon
  surname: Melov
  fullname: Melov, Simon
  organization: Buck Institute for Research on Aging
BackLink https://www.ncbi.nlm.nih.gov/pubmed/24304487$$D View this record in MEDLINE/PubMed
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ContentType Journal Article
Copyright 2013 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd.
2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
Copyright © 2014 The Anatomical Society and John Wiley & Sons Ltd
2013 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd. 2013
Copyright_xml – notice: 2013 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd.
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– notice: Copyright © 2014 The Anatomical Society and John Wiley & Sons Ltd
– notice: 2013 The Authors. published by the Anatomical Society and John Wiley & Sons Ltd. 2013
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ISSN 1474-9718
1474-9726
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IsDoiOpenAccess true
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Issue 2
Keywords postmitotic
DNA methylation
genomics
epigenome
skeletal muscle
human aging
Language English
License Attribution
http://creativecommons.org/licenses/by/3.0
2013 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.
This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.
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Snippet Summary A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report...
A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report for the...
Summary A decline in skeletal muscle mass and function with aging is well recognized, but remains poorly characterized at the molecular level. Here, we report...
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SourceType Open Access Repository
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StartPage 360
SubjectTerms Adolescent
Adult
Aged
Aging - genetics
Base Composition - genetics
CpG Islands
DNA methylation
DNA Methylation - genetics
epigenome
Gene Expression Regulation
Gene Ontology
Genome, Human - genetics
genomics
human aging
Humans
Male
Muscle, Skeletal - metabolism
Original
postmitotic
Signal Transduction - genetics
skeletal muscle
Young Adult
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Title Genome‐wide DNA methylation changes with age in disease‐free human skeletal muscle
URI https://onlinelibrary.wiley.com/doi/abs/10.1111%2Facel.12180
https://www.ncbi.nlm.nih.gov/pubmed/24304487
https://www.proquest.com/docview/1505475747
https://www.proquest.com/docview/1507191701
https://pubmed.ncbi.nlm.nih.gov/PMC3954952
Volume 13
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