Shared signatures of social stress and aging in peripheral blood mononuclear cell gene expression profiles
Article first published online: 23 JUN 2014
© 2014 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.
Volume 13, Issue 5, pages 954–957, October 2014
How to Cite
Snyder-Mackler, N., Somel, M. and Tung, J. (2014), Shared signatures of social stress and aging in peripheral blood mononuclear cell gene expression profiles. Aging Cell, 13: 954–957. doi: 10.1111/acel.12239
- Issue published online: 19 SEP 2014
- Article first published online: 23 JUN 2014
- Manuscript Accepted: 23 MAY 2014
- National Institutes of Health. Grant Numbers: 1R01-GM102562, P30-AG034424, T32AG000139-25
- National Science Foundation. Grant Number: SMA-1306134
- European Molecular Biology Organization. Grant Number: EMBO ALTF 1475–2010
- The Scientific and Technological Research Council of Turkey. Grant Number: TÜBİTAK 2232, project no: 114C040
- gene expression;
- social stress
Chronic social stress is a predictor of both aging-related disease and mortality risk. Hence, chronic stress has been hypothesized to directly exacerbate the process of physiological aging. Here, we evaluated this hypothesis at the level of gene regulation. We compared two data sets of genome-wide gene expression levels in peripheral blood mononuclear cells (PBMCs): one that captured aging effects and another that focused on chronic social stress. Overall, we found that the direction, although not necessarily the magnitude, of significant gene expression changes tends to be shared between the two data sets. This overlap was observable at three levels: (i) individual genes; (ii) general functional categories of genes; and (iii) molecular pathways implicated in aging. However, we also found evidence that heterogeneity in PBMC composition limits the power to detect more extensive similarities, suggesting that our findings reflect an underestimate of the degree to which age and social stress influence gene regulation in parallel. Cell type-specific data on gene regulation will be important to overcome this limitation in the future studies.