Journal
SCIENTIFIC REPORTS
Volume 8, Issue -, Pages -Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/s41598-018-24653-z
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- AmorePacific Corporation, Yongin, Republic of Korea [2014-51-0445]
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Psychological stress (PS) increases endogenous glucocorticoids (GC) by activating the hypothalamic-pituitary-adrenal axis. The negative effects of GC on skin barrier function under PS have been well-established. However, endogenous GC can also be active when cortisone (inactive form) is converted to cortisol (active form) by 11 beta-hydroxysteroid dehydrogenase type I (11 beta-HSD1) in the peripheral tissue. Here, we evaluated the changes in 11 beta-HSD1 and barrier function under PS. Elevated 11 beta-HSD1 in oral mucosa correlated with increased cortisol in the stratum corneum and deteriorated barrier function. Expression of 11 beta-HSD1 in the oral mucosa correlated with that in the epidermal keratinocytes. We further investigated whether barrier function improved when PS was relieved using a selective serotonin reuptake inhibitor (SSRI) in patients with anxiety. Decreased 11 beta-HSD1 and improved barrier function were observed after SSRI treatment. The collective findings suggest that elevated 11 beta-HSD1 under PS increases the level of cutaneous GC and eventually impairs barrier function. PS-alleviating drugs, such as SSRI, may help to treat PS-aggravated skin diseases.
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