| First Author | Kim BJ | Year | 2021 |
| Journal | Int J Mol Sci | Volume | 22 |
| Issue | 11 | PubMed ID | 34072239 |
| Mgi Jnum | J:331217 | Mgi Id | MGI:6751152 |
| Doi | 10.3390/ijms22115750 | Citation | Kim BJ, et al. (2021) Increased Expression of 11beta-Hydroxysteroid Dehydrogenase Type 1 Contributes to Epidermal Permeability Barrier Dysfunction in Aged Skin. Int J Mol Sci 22(11) |
| abstractText | Inactive cortisone is converted into active cortisol by 11beta-hydroxysteroid dehydrogenase type 1 (11beta-HSD1). Excessive levels of active glucocorticoids could deteriorate skin barrier function; barrier impairment is also observed in aged skin. In this study, we aimed to determine whether permeability barrier impairment in the aged skin could be related to increased 11beta-HSD1 expression. Aged humans (n = 10) showed increased cortisol in the stratum corneum (SC) and oral epithelium, compared to young subjects (n = 10). 11beta-HSD1 expression (as assessed via immunohistochemical staining) was higher in the aged murine skin. Aged hairless mice (56-week-old, n = 5) manifested greater transepidermal water loss, lower SC hydration, and higher levels of serum inflammatory cytokines than the young mice (8-week-old, n = 5). Aged 11beta-HSD1 knockout mice (n = 11), 11beta-HSD1 inhibitor (INHI)-treated aged wild type (WT) mice (n = 5) and young WT mice (n = 10) exhibited reduced SC corticosterone level. Corneodesmosome density was low in WT aged mice (n = 5), but high in aged 11beta-HSD1 knockout and aged INHI-treated WT mice. Aged mice exhibited lower SC lipid levels; this effect was reversed by INHI treatment. Therefore, upregulation of 11beta-HSD1 in the aged skin increases the active-glucocorticoid levels; this suppresses SC lipid biosynthesis, leading to impaired epidermal permeability barrier. |
