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UVB induces epidermal 11 β ‐hydroxysteroid dehydrogenase type 1 activity in vivo
Author(s) -
Tiganescu Ana,
Hupe Melanie,
Jiang Yan J.,
Celli Anna,
Uchida Yoshikazu,
Mauro Theodora M.,
Bikle Daniel D.,
Elias Peter M.,
Holleran Walter M.
Publication year - 2015
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/exd.12682
Subject(s) - transepidermal water loss , dehydrogenase , 11β hydroxysteroid dehydrogenase type 1 , in vivo , biology , endocrinology , cortisone , medicine , glucocorticoid , enzyme , microbiology and biotechnology , chemistry , biochemistry , genetics , stratum corneum
Detrimental consequences of ultraviolet radiation ( UVR ) in skin include photoageing, immunosuppression and photocarcinogenesis, processes also significantly regulated by local glucocorticoid ( GC ) availability. In man, the enzyme 11 β ‐hydroxysteroid dehydrogenase type 1 (11 β ‐ HSD 1) generates the active GC cortisol from cortisone (or corticosterone from 11‐dehydrocorticosterone in rodents). 11 β ‐ HSD 1 oxo‐reductase activity requires the cofactor NADPH , generated by hexose‐6‐phosphate dehydrogenase. We previously demonstrated increased 11 β ‐ HSD 1 levels in skin obtained from photoexposed versus photoprotected anatomical regions. However, the direct effect of UVR on 11 β ‐ HSD 1 expression remains to be elucidated. To investigate the cutaneous regulation of 11 β ‐ HSD 1 following UVR in vivo, the dorsal skin of female SKH 1 mice was irradiated with 50, 100, 200 and 400 mJ /cm 2 UVB . Measurement of transepidermal water loss, 11 β ‐ HSD 1 activity, mRNA /protein expression and histological studies was taken at 1, 3 and 7 days postexposure. 11 β ‐ HSD 1 and hexose‐6‐phosphate dehydrogenase mRNA expression peaked 1 day postexposure to 400 mJ /cm 2 UVB before subsequently declining (days 3 and 7). Corresponding increases in 11 β ‐ HSD 1 protein and enzyme activity were observed 3 days postexposure coinciding with reduced GC receptor mRNA expression. Immunofluorescence studies revealed 11 β ‐ HSD 1 localization to hyperproliferative epidermal keratinocytes in UVB ‐exposed skin. 11 β ‐ HSD 1 expression and activity were also induced by 200 and 100 (but not 50) mJ /cm 2 UVB and correlated with increased transepidermal water loss (indicative of barrier disruption). UVB ‐induced 11 β ‐ HSD 1 activation represents a novel mechanism that may contribute to the regulation of cutaneous responses to UVR exposure.