Cited by 123Stress Responses and CortisolGenetic Associations and EpidemiologyNeurotransmitter Receptor Influence on Behavior

Elevating the perspective on human stress genomics

Open access
Cole, Steve W.·2010·Psychoneuroendocrinology

Abstract

Functional genomics strategies have been slow to penetrate research on human stress and coping, but recent conceptual advances have yielded a raft of new findings relating social and psychological conditions to broad alterations in human gene expression. This article reviews the field of human stress genomics, analyzes some of the conceptual and technical issues that initially hampered its progress, and outlines an abstractionist approach to genomic data analysis that has revealed a surprisingly consistent pattern of human transcriptional responses to diverse types of socio-environmental adversity. This field is now poised for another round of significant advances as research begins to incorporate the effects of DNA polymorphism, target a broader array of healthy and diseased tissues, and identify general teleologic and regulatory themes by pooling results over a growing body of studies analyzing the human transcriptional response to stress.

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Crossref · 10.1016/j.psyneuen.2010.06.008

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  • Whole gene programs or gene profiles, such as the CTRA, can be activated by adverse social conditions.

    “whole gene programs or gene profiles, such as the CTRA, can be activated by adverse social conditions”
  • Across diverse forms of adversity, a common conserved transcriptional response to adversity (CTRA) has emerged, including increased expression of proinflammatory genes and decreased expression of genes involved in Type I interferon innate antiviral responses and IgG antibody synthesis.

    “Across these diverse forms of adversity, a common pattern of conserved transcriptional response to adversity (CTRA) has emerged, including increased expression of proinflammatory genes and decreased expression of genes involved in Type I interferon innate antiviral responses and IgG antibody synthesis [3], [5], [28].”

    From Human Social Genomics (2014) · cites this paper as [28]

  • The sympathetic nervous system allows the CNS to steer innate immune responses between proinflammatory and antiviral phenotypes.

    “the SNS allows the CNS to 'steer' innate immune responses between proinflammatory and antiviral phenotypes”

    From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Cole, 2010

  • Adrenergic signaling suppresses antiviral type I interferon genes and upregulates IL1B, TNF, and IL6, increasing systemic inflammatory activity.

    “Such adrenergic signaling suppresses transcription of antiviral type I interferon genes, as previously discussed elsewhere (Cole et al, 1998), and also upregulates transcription of the proinflammatory immune response genes IL1B, TNF, and IL6, leading to increase in systemic inflammatory activity (Cole, 2010).”

    From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Cole, 2010

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Research works printed but not linked: 5

  1. Morita K Saito T Ohta M Ohmori T Kawai K Teshima-Kondo S Rokutan K 2005 Expression analysis of psychological stress-associated genes in peripheral blood leukocytes Neurosci Lett 381 1–2 57 62 15882790 One of the first studies of the human transcriptional response to stress, this paper analyzed the effects of a truly acute stressor (Ph.D. thesis defense!) on a targeted subset of the human transcriptome
  2. Cole SW Hawkley LC Arevalo JM Sung CY Rose RM Cacioppo JT 2007 Social regulation of gene expression in human leukocytes Genome Biol 8 R189 1 13 PMC2375027 17854483 This pivotal study provided the first indication that long-term social adversity is associated with broad transcriptional alterations in the human immune system. Several recurring biological themes initially emerged in this paper, including indications of glucocorticoid resistance, NF-κBlinked chronic inflammation, and suppression of innate antiviral responses
  3. Miller GE Chen E Fok AK Walker H Lim A Nicholls EF Cole S Kobor MS 2009 Low early-life social class leaves a biological residue manifested by decreased glucocorticoid and increased proinflammatory signaling Proc Natl Acad Sci U S A 106 34 14716 21 19617551 PMC2732821 A remarkable study showing that early life social conditions can leave an enduring imprint on human gene expression decades later in adulthood. This is one of a number of studies documenting a pro-inflammatory shift in leukocyte gene expression in response to socio-environmental adversity
  4. Cole SW 2009 Social regulation of human gene expression Current Directions in Psychological Science 18 3 132 137 PMC3020789 21243077 In addition to surveying the broad field of social genomics, this review develops some of the theoretical implications of socio-environmental gene regulation for long-term individual developmental trajectories
  5. Cole S Arevalo J Takahashi R Sloan EK Lutgendorf S Sood AK Sheridan JF Seeman T 2010 Computational identification of gene-social environment interaction at the human IL6 locus Proc Natl Acad Sci U S A 107 5681 5686 20176930 PMC2851818 Combining stress genomics with analyses of genetic polymorphism, this study presents a new computational strategy for discovering gene-environment interactions. This study also mapped a new transcription factor pathway through which stress can regulate gene expression

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Authors
Cole, S. W.
Affiliations
University of California, Los Angeles (US)
Corresponding author
Cole, Steve W.
Venue
Psychoneuroendocrinology
Publisher
Elsevier BV
Published
2010-08
Volume
35
Issue
7
Pages
955-962
ISSN
0306-4530 (ISSN-L)
OpenAlex
W2169362360
Cited by
123
References
54
Citations by year
2026: 2 · 2025: 14 · 2024: 7 · 2023: 7 · 2022: 6 · 2021: 5 · 2020: 10 · 2019: 7 · 2018: 4 · 2017: 8 · 2016: 13 · 2015: 7 · 2014: 10 · 2013: 9 · 2012: 10
FWCI
0.65
Type
journal article
Language
en
Open access
Locations
  • Psychoneuroendocrinology (publishedVersion)
  • PubMed (publishedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • National Institute on Aging (AG-10415, AG107265, P60AG010415)
  • National Cancer Institute (R01CA116778, CA-116778)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Genetic Associations and Epidemiology
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
Keywords
gene expression, coping, DNA polymorphism, functional genomics, gene expression regulation, psychological stress
MeSH terms
Humans, Polymorphism, Genetic, Social Environment, Stress, Psychological, Transcription, Genetic, Gene Expression Profiling, Genomics

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