Author
Listed:
- Lindsay M. Reynolds
(Wake Forest School of Medicine
Wake Forest School of Medicine)
- Jackson R. Taylor
(Wake Forest School of Medicine
J. Paul Sticht Center on Aging, Wake Forest School of Medicine)
- Jingzhong Ding
(Wake Forest School of Medicine
J. Paul Sticht Center on Aging, Wake Forest School of Medicine
Wake Forest School of Medicine)
- Kurt Lohman
(Wake Forest School of Medicine
Wake Forest School of Medicine)
- Craig Johnson
(University of Washington)
- David Siscovick
(University of Washington
University of Washington
Cardiovascular Health Research Unit, University of Washington)
- Gregory Burke
(Wake Forest School of Medicine)
- Wendy Post
(Johns Hopkins University)
- Steven Shea
(Columbia University Medical Center
Columbia University Medical Center)
- David R. Jacobs Jr.
(School of Public Health, University of Minnesota)
- Hendrik Stunnenberg
(Nijmegen Centre for Molecular Life Sciences (NCMLS))
- Stephen B. Kritchevsky
(Wake Forest School of Medicine
J. Paul Sticht Center on Aging, Wake Forest School of Medicine
Wake Forest School of Medicine)
- Ina Hoeschele
(Virginia Bioinformatics Institute, Virginia Tech)
- Charles E. McCall
(J. Paul Sticht Center on Aging, Wake Forest School of Medicine
Wake Forest School of Medicine
Department of Molecular Medicine
Translational Science Institute, Wake Forest School of Medicine)
- David M. Herrington
(Wake Forest School of Medicine)
- Russell P. Tracy
(University of Vermont)
- Yongmei Liu
(Wake Forest School of Medicine
Wake Forest School of Medicine
J. Paul Sticht Center on Aging, Wake Forest School of Medicine)
Abstract
Age-related variations in DNA methylation have been reported; however, the functional relevance of these differentially methylated sites (age-dMS) are unclear. Here we report potentially functional age-dMS, defined as age- and cis-gene expression-associated methylation sites (age-eMS), identified by integrating genome-wide CpG methylation and gene expression profiles collected ex vivo from circulating T cells (227 CD4+ samples) and monocytes (1,264 CD14+ samples, age range: 55–94 years). None of the age-eMS detected in 227 T-cell samples are detectable in 1,264 monocyte samples, in contrast to the majority of age-dMS detected in T cells that replicated in monocytes. Age-eMS tend to be hypomethylated with older age, located in predicted enhancers and preferentially linked to expression of antigen processing and presentation genes. These results identify and characterize potentially functional age-related methylation in human T cells and monocytes, and provide novel insights into the role age-dMS may have in the aging process.
Suggested Citation
Lindsay M. Reynolds & Jackson R. Taylor & Jingzhong Ding & Kurt Lohman & Craig Johnson & David Siscovick & Gregory Burke & Wendy Post & Steven Shea & David R. Jacobs Jr. & Hendrik Stunnenberg & Stephe, 2014.
"Age-related variations in the methylome associated with gene expression in human monocytes and T cells,"
Nature Communications, Nature, vol. 5(1), pages 1-8, December.
Handle:
RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6366
DOI: 10.1038/ncomms6366
Download full text from publisher
Citations
Citations are extracted by the
CitEc Project, subscribe to its
RSS feed for this item.
Cited by:
- Zhaohui Qin & Ben Li & Karen N. Conneely & Hao Wu & Ming Hu & Deepak Ayyala & Yongseok Park & Victor X. Jin & Fangyuan Zhang & Han Zhang & Li Li & Shili Lin, 2016.
"Statistical Challenges in Analyzing Methylation and Long-Range Chromosomal Interaction Data,"
Statistics in Biosciences, Springer;International Chinese Statistical Association, vol. 8(2), pages 284-309, October.
- Tianyu Zhu & Huige Tong & Zhaozhen Du & Stephan Beck & Andrew E. Teschendorff, 2024.
"An improved epigenetic counter to track mitotic age in normal and precancerous tissues,"
Nature Communications, Nature, vol. 15(1), pages 1-19, December.
- Tiago C. Silva & Juan I. Young & Lanyu Zhang & Lissette Gomez & Michael A. Schmidt & Achintya Varma & X. Steven Chen & Eden R. Martin & Lily Wang, 2022.
"Cross-tissue analysis of blood and brain epigenome-wide association studies in Alzheimer’s disease,"
Nature Communications, Nature, vol. 13(1), pages 1-16, December.
Corrections
All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:5:y:2014:i:1:d:10.1038_ncomms6366. See general information about how to correct material in RePEc.
If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.
We have no bibliographic references for this item. You can help adding them by using this form .
If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.
For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .
Please note that corrections may take a couple of weeks to filter through
the various RePEc services.