Abstract

Introduction: Previous studies have examined effects of acute psychological stress in humans on selected panels of genes. This exploratory study aimed to investigate genome-wide transcriptional activity changes in responses to acute psychological stress. Methods: The sample included 40 healthy women who participated in a previous study (22 who had a stress induced experience (experimental group) and 18 who did not (control group)). The psychological stress was induced by the Trier Social Stress Test (TSST). Psychological stress levels (measured by the Subjective Units of Distress Scale (SUDS) and the state anxiety subscale of the Spielberger State-Trait Anxiety Inventory) and hemodynamic changes (measured by blood pressure (BP) and heart rate (HR)) were assessed before and after the TSST. The peripheral blood samples obtained before and after the TSST were processed for mRNA-sequencing. Results: The mean age of the participants was 31 years (SD 11.6). The psychological and hemodynamic stress parameters indicated that the TSST successfully induced moderate but statistically significant levels of acute psychological stress in the participants of the experimental group. Compared with the participants in the control group, six genes ( BCL2L14, FAM3B, HCG26, HLA-F-AS1, LOC101928710 , and SLC22A16 ) were up-regulated and 9 genes ( ATP2C2, CA1, CRYBG3, FBXO9, HBD, SLC39A9, SNCA, STRADB , and TRMT12 ) were down-regulated among those who experienced stress induction. The IPA analysis identified one network of cell-to-cell signaling and interaction, cellular function and maintenance, and hematological system development and function. Thirteen genes out of 15 were found in this network. Conclusions: The identified genes including FAM3B, BCL2L14, SLC22A16 , and SNCA , have been proposed as the therapeutic targets of diabetes-related CVDs, certain cancers, and Parkinson’s disease, but have not previously been reported to be associated with psychological stress. Future studies are suggested to examine the pathological mechanisms by which the identified genes may mediate the association between psychological stress and adverse health outcome.

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