| First Author | Itoi-Ochi S | Year | 2016 |
| Journal | Dermatoendocrinol | Volume | 8 |
| Issue | 1 | Pages | e1119958 |
| PubMed ID | 27195053 | Mgi Jnum | J:236052 |
| Mgi Id | MGI:5804506 | Doi | 10.1080/19381980.2015.1119958 |
| Citation | Itoi-Ochi S, et al. (2016) Local corticosterone activation by 11beta-hydroxysteroid dehydrogenase 1 in keratinocytes: the role in narrow-band UVB-induced dermatitis. Dermatoendocrinol 8(1):e1119958 |
| abstractText | Keratinocytes are known to synthesize cortisol through activation of the enzyme 11beta-hydroxysteroid dehydrogenase 1 (11beta-HSD1). To confirm the function of 11beta-HSD1 in keratinocytes during inflammation in vivo, we created keratinocyte-specific-11beta-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 11beta-HSD1 following NB-UVB irradiation and found that the expression of 11beta-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-kappaB) 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 11beta-HSD1 may suppress NB-UVB-induced inflammation via inhibition of NF-kappaB activation. |
