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Author Notes:

Correspondence: Toni Whistler, taw6@cdc.gov

Disclosures: Drs. Nater, Whistler, Vernon, and Ms. Mletzko and Mr Lonergan reported no biomedical financial interests or potential conflicts of interest. Dr. Heim reports having received funding from NIMH, CDC, NARSAD, ADAA, Eli Lilly, and Novartis.

Subjects:

Research Funding:

This study was supported by a 2002 NARSAD Young Investigator Award (CH) and a PHS grant, NCRR M01-RR00039 (Emory University Hospital General Clinical Research Center). This research was supported in part by an appointment to the Research Participation Program at the Centers for Disease Control and Prevention administered by the Oak Ridge Institute for Science and Education through an interagency agreement between the U.S. Department of Energy and CDC (UMN).

Keywords:

  • Social Sciences
  • Science & Technology
  • Life Sciences & Biomedicine
  • Psychology, Biological
  • Behavioral Sciences
  • Psychology
  • Psychology, Experimental
  • Gene expression
  • Psychosocial stress
  • Peripheral blood mononuclear cell
  • Microarray
  • Biological pathways
  • Adhesion molecule expression
  • Acute psychological stress
  • Messenger-RNA
  • Receptors
  • Disorder
  • Hormone

Impact of acute psychosocial stress on peripheral blood gene expression pathways in healthy men

Tools:

Journal Title:

Biological Psychology

Volume:

Volume 82, Number 2

Publisher:

, Pages 125-132

Type of Work:

Article | Final Publisher PDF

Abstract:

We investigated peripheral blood mononuclear cell gene expression responses to acute psychosocial stress to identify molecular pathways relevant to the stress response. Blood samples were obtained from 10 healthy male subjects before, during and after (at 0, 30, and 60 min) a standardized psychosocial laboratory stressor. Ribonucleic acid (RNA) was extracted and gene expression measured by hybridization to a 20,000-gene microarray. Gene Set Expression Comparisons (GSEC) using defined pathways were used for the analysis. Forty-nine pathways were significantly changed from baseline to immediately after the stressor (p < 0.05), implicating cell cycle, cell signaling, adhesion and immune responses. The comparison between stress and recovery (measured 30 min later) identified 36 pathways, several involving stress-responsive signaling cascades and cellular defense mechanisms. These results have relevance for understanding molecular mechanisms of the physiological stress response, and might be used to further study adverse health outcomes of psychosocial stress.

Copyright information:

© 2009 Elsevier B.V.

This is an Open Access work distributed under the terms of the Creative Commons Attribution 4.0 International License (https://creativecommons.org/licenses/by/4.0/).
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