Local cortisol/corticosterone activation in skin physiology and pathology
Abstract Cortisol and corticosterone are the endogenous glucocorticoids (GCs) in humans and rodents, respectively. Systemic GC is released through the hypothalamic-pituitary-adrenal (HPA) axis in response to various stressors. Over the last decade, extra-adrenal production/activation of cortisol/cor...
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Veröffentlicht in: | Journal of dermatological science 2016-10, Vol.84 (1), p.11-16 |
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Format: | Artikel |
Sprache: | eng |
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Zusammenfassung: | Abstract Cortisol and corticosterone are the endogenous glucocorticoids (GCs) in humans and rodents, respectively. Systemic GC is released through the hypothalamic-pituitary-adrenal (HPA) axis in response to various stressors. Over the last decade, extra-adrenal production/activation of cortisol/corticosterone has been reported in many tissues. The enzyme that catalyzes the conversion of hormonally inactive cortisone/11-dehydrocorticosterone (11-DHC) into active cortisol/corticosterone in cells is 11β-hydroxysteroid dehydrogenase (11β-HSD). The 11β-HSD1 isoform is predominantly a reductase, which catalyzes nicotinamide adenine dinucleotide phosphate hydrogen-dependent conversion of cortisone/11-DHC to cortisol/corticosterone, and is widely expressed and present at the highest levels in the liver, lungs, adipose tissues, ovaries, and central nervous system. The 11β-HSD2 isoform, which catalyzes nicotinamide adenine dinucleotide+ -dependent inactivation of cortisol/corticosterone to cortisone/11-DHC, is highly expressed in distal nephrons, the colon, sweat glands, and the placenta. In healthy skin, 11β-HSD1 is expressed in the epidermis and in dermal fibroblasts. On the other hand, 11β-HSD2 is expressed in sweat glands but not in the epidermis. The role of 11β-HSD in skin physiology and pathology has been reported recently. In this review, we summarize the recently reported role of 11β-HSD in the skin, focusing on its function in cell proliferation, wound healing, inflammation, and aging. |
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ISSN: | 0923-1811 1873-569X |
DOI: | 10.1016/j.jdermsci.2016.06.014 |