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Exertional heat injury and gene expression changes: a DNA microarray analysis study.

Larry A Sonna1, C Bruce Wenger, Scott Flinn

  • 1Thermal and Mountain Medicine Div., United States Army Research Institute of Environmental Medicine, Natick, MA 01760, USA. larry.sonna@na.amedd.army.mil

Journal of Applied Physiology (Bethesda, Md. : 1985)
|February 24, 2004
PubMed
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Exertional heat injury (EHI) triggers a wide gene expression response in blood cells, going beyond simple heat stress. This suggests EHI results from multiple interacting factors, not just heat alone.

Area of Science:

  • Molecular biology
  • Human physiology
  • Stress response

Background:

  • Exertional heat injury (EHI) is a serious condition affecting individuals during intense physical activity in hot environments.
  • Previous research has identified heat shock responses in vitro, but the in vivo response during EHI is less understood.
  • Understanding the molecular basis of EHI is crucial for developing effective prevention and treatment strategies.

Purpose of the Study:

  • To investigate gene expression changes in peripheral blood mononuclear cells (PBMCs) of individuals with EHI.
  • To compare the in vivo EHI gene expression profile with previously established in vitro heat shock responses.
  • To explore the molecular mechanisms underlying EHI and identify potential contributing factors.

Main Methods:

Related Experiment Videos

  • Collected peripheral blood mononuclear cell (PBMC) RNA from Marine recruits diagnosed with EHI and age/gender-matched controls.
  • Utilized Affymetrix arrays for gene expression analysis on samples taken at multiple time points during and after EHI.
  • Compared gene expression data from EHI patients against control samples obtained before and after a strenuous heat-based exercise ('The Crucible').
  • Main Results:

    • Identified 361 transcripts with increased expression and 331 transcripts with decreased expression (twofold or greater) in EHI patients.
    • Observed changes in heat shock proteins and non-heat shock proteins, consistent with in vitro heat shock responses.
    • Detected alterations in interferon-induced sequences and other nonspecific stress response genes not previously linked to in vitro heat shock.

    Conclusions:

    • Exertional heat injury (EHI) induces a broad molecular stress response detectable in PBMCs.
    • Heat stress alone cannot fully explain all observed gene expression changes during EHI.
    • The findings support the hypothesis that EHI arises from the cumulative impact of multiple interacting adverse stimuli.