The acute and temporary modulation of PERIOD genes by hydrocortisone in healthy subjects.
Identifieur interne : 000077 ( Main/Exploration ); précédent : 000076; suivant : 000078The acute and temporary modulation of PERIOD genes by hydrocortisone in healthy subjects.
Auteurs : Türkan Yurtsever [Allemagne] ; Thomas M. Schilling [Allemagne] ; Monika Kölsch [Allemagne] ; Jonathan D. Turner [Luxembourg (pays)] ; Jobst Meyer [Allemagne] ; Hartmut Sch Chinger [Allemagne] ; Andrea B. Schote [Allemagne]Source :
- Chronobiology international [ 1525-6073 ] ; 2016.
Abstract
The physiological stress system and the circadian clock system communicate with each other at different signaling levels. The steroid hormone cortisol, the end-effector of the hypothalamus-pituitary-adrenal axis, is released in response to stress and acts as a mediator in circadian rhythms. We determined the effect of escalating cortisol doses on the expression of PERIOD genes (PER1, PER2 and PER3) in healthy subjects and analyzed whether the glucocorticoid receptor (GR) is involved in the cortisol-mediated PERIOD gene expression. Forty participants (50% males and 50% females) were randomly assigned to groups receiving a saline placebo solution or 3 mg, 6 mg, 12 mg and 24 mg of hydrocortisone. Blood was drawn every 15 min to measure quantitative gene expression of PER1, PER2 and PER3. A potential role of the GR was determined by an ex vivo study stimulating whole blood with hydrocortisone and RU486 (a GR antagonist). As a result, moderate doses of hydrocortisone produced an acute and temporary induction of PER1 and PER3 mRNA levels, whereas PER2 was not responsive to the hormone administration. The cortisol-dependent induction of PER1 was blocked by the GR antagonist in whole blood after treatment with hydrocortisone and RU486 ex vivo. In conclusion, acute pharmacological stress modulated the expression of PER1 and PER3 in whole blood temporarily in our short-term sampling design, suggesting that these circadian genes mediate stable molecular mechanisms in the periphery.
DOI: 10.1080/07420528.2016.1211668
PubMed: 27485028
Affiliations:
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Schilling</name><affiliation wicri:level="1"><nlm:affiliation>b Department of Clinical Psychophysiology , Institute of Psychobiology, University of Trier , Trier , Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>b Department of Clinical Psychophysiology , Institute of Psychobiology, University of Trier , Trier </wicri:regionArea><wicri:noRegion>Trier </wicri:noRegion><wicri:noRegion>Trier </wicri:noRegion><wicri:noRegion>Trier </wicri:noRegion></affiliation></author><author><name sortKey="Kolsch, Monika" sort="Kolsch, Monika" uniqKey="Kolsch M" first="Monika" last="Kölsch">Monika Kölsch</name><affiliation wicri:level="1"><nlm:affiliation>b Department of Clinical Psychophysiology , Institute of Psychobiology, University of Trier , Trier , Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>b Department of Clinical Psychophysiology , Institute of Psychobiology, University of Trier , Trier </wicri:regionArea><wicri:noRegion>Trier </wicri:noRegion><wicri:noRegion>Trier </wicri:noRegion><wicri:noRegion>Trier </wicri:noRegion></affiliation></author><author><name sortKey="Turner, Jonathan D" sort="Turner, Jonathan D" uniqKey="Turner J" first="Jonathan D" last="Turner">Jonathan D. 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Schote</name><affiliation wicri:level="1"><nlm:affiliation>a Department of Neurobehavioral Genetics , Institute of Psychobiology, University of Trier , Trier , Germany.</nlm:affiliation><country xml:lang="fr">Allemagne</country><wicri:regionArea>a Department of Neurobehavioral Genetics , Institute of Psychobiology, University of Trier , Trier </wicri:regionArea><wicri:noRegion>Trier </wicri:noRegion><wicri:noRegion>Trier </wicri:noRegion><wicri:noRegion>Trier </wicri:noRegion></affiliation></author></analytic><series><title level="j">Chronobiology international</title><idno type="eISSN">1525-6073</idno><imprint><date when="2016" type="published">2016</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The physiological stress system and the circadian clock system communicate with each other at different signaling levels. The steroid hormone cortisol, the end-effector of the hypothalamus-pituitary-adrenal axis, is released in response to stress and acts as a mediator in circadian rhythms. We determined the effect of escalating cortisol doses on the expression of PERIOD genes (PER1, PER2 and PER3) in healthy subjects and analyzed whether the glucocorticoid receptor (GR) is involved in the cortisol-mediated PERIOD gene expression. Forty participants (50% males and 50% females) were randomly assigned to groups receiving a saline placebo solution or 3 mg, 6 mg, 12 mg and 24 mg of hydrocortisone. Blood was drawn every 15 min to measure quantitative gene expression of PER1, PER2 and PER3. A potential role of the GR was determined by an ex vivo study stimulating whole blood with hydrocortisone and RU486 (a GR antagonist). As a result, moderate doses of hydrocortisone produced an acute and temporary induction of PER1 and PER3 mRNA levels, whereas PER2 was not responsive to the hormone administration. The cortisol-dependent induction of PER1 was blocked by the GR antagonist in whole blood after treatment with hydrocortisone and RU486 ex vivo. In conclusion, acute pharmacological stress modulated the expression of PER1 and PER3 in whole blood temporarily in our short-term sampling design, suggesting that these circadian genes mediate stable molecular mechanisms in the periphery.</div></front></TEI><affiliations><list><country><li>Allemagne</li><li>Luxembourg (pays)</li></country></list><tree><country name="Allemagne"><noRegion><name sortKey="Yurtsever, Turkan" sort="Yurtsever, Turkan" uniqKey="Yurtsever T" first="Türkan" last="Yurtsever">Türkan Yurtsever</name></noRegion><name sortKey="Kolsch, Monika" sort="Kolsch, Monika" uniqKey="Kolsch M" first="Monika" last="Kölsch">Monika Kölsch</name><name sortKey="Meyer, Jobst" sort="Meyer, Jobst" uniqKey="Meyer J" first="Jobst" last="Meyer">Jobst Meyer</name><name sortKey="Sch Chinger, Hartmut" sort="Sch Chinger, Hartmut" uniqKey="Sch Chinger H" first="Hartmut" last="Sch Chinger">Hartmut Sch Chinger</name><name sortKey="Schilling, Thomas M" sort="Schilling, Thomas M" uniqKey="Schilling T" first="Thomas M" last="Schilling">Thomas M. Schilling</name><name sortKey="Schote, Andrea B" sort="Schote, Andrea B" uniqKey="Schote A" first="Andrea B" last="Schote">Andrea B. Schote</name></country><country name="Luxembourg (pays)"><noRegion><name sortKey="Turner, Jonathan D" sort="Turner, Jonathan D" uniqKey="Turner J" first="Jonathan D" last="Turner">Jonathan D. Turner</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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