Effects of Psychosocial Stress on the Gene Expression of the Clock Genes hPER1 and hPER2 in Humans

All biological processes recurring daily, also known as circadian-controlled processes, are governed by the so-called circadian clock, a self-sustained time-keeping system controlling rhythmic behavioral, biochemical and physiological processes. In other words, the circadian clock affects the sleep-wake cycle, body temperature, hormone secretion, enzyme activity, renal blood flow, heart rate, and various other physiological activities as well as the regulation of the cell cycle and of apoptosis.

In mammals, the cogwheels of this clock are the so-called clock genes which control their own expression via several feedback loops. One of these genes is hPER1, a clock gene which disposes of a glucocorticoid-responsive element and might therefore be influenced by glucocorticoids.

In humans, stress is associated with an increase in the glucocorticoid cortisol and is seen as a major factor in the etiology of numerous mental health problems. For this reason, the goal of this paper was to investigate the putative cortisol-mediated influence of acute and chronic psychosocial stress on the gene expression of hPER1 as well as hPER2, another related clock gene from the same family.

The authors applied laboratory psychosocial stress to thirty-one healthy men and measured cortisol as well as mRNA levels of hPER1 and hPER2. The investigation took place on two consecutive days in the laboratories of the Department of Clinical Psychology and Psychotherapy of the University of Zurich. mRNA levels of hPER1 as well as hPER2 were assessed in oral mucosa and analyzed in the biochemical laboratory of the Psychological Institute of the University of Zurich. The quantitative real-time PCR was conducted and cortisol samples were collected using Salivettes.

The main findings suggest that acute psychosocial stress influences the expression of hPER1 and hPER2 dependent on the subjective experience of chronic stress. Therefore, it’s concluded that the reactivity to acute stress on the gene expression level of these two genes differs significantly between subjects with high chronic stress compared to subjects with low chronic stress.

Article by Elvira A. Abbruzzese, et al, from Switzerland.

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