Cited by 129Telomeres, Telomerase, and SenescenceCircadian rhythm and melatoninSleep and Work-Related Fatigue

Partial sleep deprivation activates the DNA damage response (DDR) and the senescence-associated secretory phenotype (SASP) in aged adult humans

Open access
Carroll, Judith E., Cole, Steven W., Seeman, Teresa E., Breen, Elizabeth C., Witarama, Tuff, Arevalo, Jesusa M.G., Ma, Jeffrey, Irwin, Michael R.·2016·Brain, Behavior, and Immunity

Abstract

Age-related disease risk has been linked to short sleep duration and sleep disturbances; however, the specific molecular pathways linking sleep loss with diseases of aging are poorly defined. Key cellular events seen with aging, which are thought to contribute to disease, may be particularly sensitive to sleep loss. We tested whether one night of partial sleep deprivation (PSD) would increase leukocyte gene expression indicative of DNA damage responses (DDR), the senescence-associated secretory phenotype (SASP), and senescence indicator p16(INK4a) in older adult humans, who are at increased risk for cellular senescence. Community-dwelling older adults aged 61-86years (n=29; 48% male) underwent an experimental partial sleep deprivation (PSD) protocol over 4 nights, including adaptation, an uninterrupted night of sleep, partial sleep deprivation (sleep restricted 3-7AM), and a subsequent full night of sleep. Blood samples were obtained each morning to assess peripheral blood mononuclear cell (PBMC) gene expression using Illumina HT-12 arrays. Analyses of microarray results revealed that SASP (p<.05) and DDR (p=.08) gene expression were elevated from baseline to PSD nights. Gene expression changes were also observed from baseline to PSD in NFKB2, NBS1 and CHK2 (all p's<.05). The senescence marker p16(INK4a) (CDKN2A) was increased 1day after PSD compared to baseline (p<.01), however confirmatory RT-PCR did not replicate this finding. One night of partial sleep deprivation activates PBMC gene expression patterns consistent with biological aging in this older adult sample. PSD enhanced the SASP and increased the accumulation of damage that initiates cell cycle arrest and promotes cellular senescence. These findings causally link sleep deprivation to the molecular processes associated with biological aging.

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Crossref · 10.1016/j.bbi.2015.08.024

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  • Dietary and lifestyle habits and exposure to pollutants can increase oxidative stress, upregulate mitogenic signaling pathways, and cause genomic and epigenomic perturbations that induce the senescence-associated secretory phenotype.

    “dietary and lifestyle habits, as well as exposure to a variety of different pollutants, can increase oxidative stress, upregulate mitogenic signaling pathways and cause genomic and epigenomic perturbations8,60,62,63 that can induce the SASP.”

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Research works printed but not linked: 1

  1. [12]Colten HR Altevogt BM Research I of MUS. C on SM and. Sleep disorders and sleep deprivation: an unmet public health problem 2006 National Academies Press 20669438

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Authors
Carroll, J. E., Cole, S. W., Seeman, T. E., Breen, E. C., Witarama, T., Arevalo, J. M. G., Ma, J., & Irwin, M. R.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Carroll, Judith E.
Venue
Brain, Behavior, and Immunity
Publisher
Elsevier BV
Published
2016-01
Volume
51
Pages
223-229
ISSN
0889-1591 (ISSN-L)
OpenAlex
W1279301897
Cited by
129
References
70
Citations by year
2026: 10 · 2025: 15 · 2024: 26 · 2023: 15 · 2022: 11 · 2021: 10 · 2020: 12 · 2019: 14 · 2018: 7 · 2017: 2 · 2016: 7
FWCI
3.89
Type
journal article
Language
en
Open access
Locations
  • Brain Behavior and Immunity (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
  • eScholarship (California Digital Library) (submittedVersion)
Funders
  • National Institute on Aging (R01 AG034588)
  • UCLA Older Americans Independence Center (P30 AG028748)
  • UCLA Clinical and Translational Science Institute (UL1TR000124)
  • National Institute of Mental Health (T32 MH019925)
  • NIA (K01 AG044462)
  • American Sleep Medicine Foundation
  • Cousins Center for Psychoneuroimmunology
  • USC/UCLA Center on Biodemography & Population Health (P30 AG017265)
  • UCLA Neuroscience Genomics Core Laboratory
Topics
  • Health Sciences › Medicine › Physiology › Telomeres, Telomerase, and Senescence
  • Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Circadian rhythm and melatonin
  • Social Sciences › Psychology › Experimental and Cognitive Psychology › Sleep and Work-Related Fatigue
Keywords
sleep restriction, DNA damage response, senescence-associated secretory phenotype, cellular senescence, p16INK4a, leukocyte gene expression, peripheral blood mononuclear cells, aging, NFKB2, NBS1, Chk2, age-related disease risk, older adults
MeSH terms
Aged, Aged, 80 and over, Aging, DNA Damage, Female, Humans, Leukocytes, Mononuclear, Male, Middle Aged, Phenotype, Sleep Deprivation, Cellular Senescence, Genes, p16

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