Local corticosterone activation by 11β-hydroxysteroid dehydrogenase 1 in keratinocytes: the role in narrow-band UVB-induced dermatitis. Issue 1 (1st January 2016)

• Record Type: Journal Article
• Authors: Itoi-Ochi, Saori; Terao, Mika; Murota, Hiroyuki; Katayama, Ichiro
• Is Part Of: Dermato-endocrinology. Volume 8:Issue 1(2016)
• Publication Date: 2016-01-01
• Subjects: corticosterone -- inflammation -- keratinocytes -- narrow-band UVB -- 11β-hydroxysteroid dehydrogenase 1; Skin -- Diseases -- Periodicals; Skin Diseases -- Periodicals; Skin -- Periodicals; Endocrine System -- physiopathology -- Periodicals; Skin -- Diseases; Periodicals; Electronic journals; 616.5
• DOI: 10.1080/19381980.2015.1119958
• Languages: English
• ISSNs: 1938-1972

Abstract

ABSTRACT: Keratinocytes are known to synthesize cortisol through activation of the enzyme 11β-hydroxysteroid dehydrogenase 1 (11β-HSD1). To confirm the function of 11β-HSD1 in keratinocytes during inflammation in vivo, we created keratinocyte-specific-11β-HSD1 knockout mice ( K5-Hsd11b1-KO mice) and analyzed the response to narrow-band ultraviolet B (NB-UVB) irradiation. Firstly, we measured the mRNA and protein levels of 11β-HSD1 following NB-UVB irradiation and found that the expression of 11β-HSD1 in keratinocytes of mouse ear skin was enhanced at 3 and 24 hours after 250 mJ/cm 2, 500 mJ/cm 2, 1 J/cm 2, and 2 J/cm 2 NB-UVB irradiation. Next, we determined that 24 hours after exposure to 1 J/cm 2 NB-UVB irradiation, the numbers of F4/80-, CD45-, and Gr-1-positive cells were increased in K5-Hsd11b1-KO mice compared to wild type (WT) mice. Furthermore, the expression of the chemokine (C-X-C-motif) ligand 1 (CXCL1) and interleukin (IL)-6 was also significantly enhanced in NB-UVB-irradiated K5-Hsd11b1-KO mice compared with WT mice. In addition, activation of nuclear factor-kappa B (NF-κB) after NB-UVB irradiation was enhanced in K5-Hsd11b1-KO mice compared to that in WT mice. Thus, NB-UVB-induced inflammation is augmented in K5-Hsd11b1-KO mice compared with WT mice. These results indicate that 11β-HSD1 may suppress NB-UVB-induced inflammation via inhibition of NF-κB activation.