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      Increased 11β-hydroxysteroid dehydrogenase type 1 contributes to barrier dysfunction in aged skin = Increased 11β-hydroxysteroid dehydrogenase type 1 contributes to barrier dysfunction in aged skin

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      https://www.riss.kr/link?id=A106456433

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      Background: 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts inactive cortisone into cortisol, an active form, and is expressed by several tissues including the skin. Excessive active glucocorticoid (GC) deteriorates skin barrier function.
      Objectives: To find out if 11β-HSD1 affects on the barrier function in aged skin.
      Methods: We have performed human and in vivo studies. We measured cortisol in stratum corneum (SC) and oral epithelium of the elderly and young. Hairless mice were used for 11β-HSD1 immunohistochemistry staining of skin and measuring skin barrier function and serum cytokines. 11β-HSD1 knock-out (KO) mice and its wild-type were used for measuring lipid synthesis related enzyme.
      Results: Cortisol levels were elevated in SC and oral epithelium of the elderly rather than young. The 11β -HSD1 expression was increased in immunohistochemistry stain of aged mice skin. Aged mice showed decreased transepidermal water loss (TEWL) and SC hydration, and increased SC integrity than young. Serum inflammatory cytokines including interleukin-1α, -4, -10, -31 and tumor necrosis factor-α were increased in aged mice than young. The expressions of lipid synthesis related enzymes in epidermis were elevated in KO mice and topical 11β -HSD1 inhibitor applied mice.
      Conclusion: 11β-HSD1 expression is elevated in aged skin. It increases active GC and then deteriorates skin barrier function.
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      Background: 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts inactive cortisone into cortisol, an active form, and is expressed by several tissues including the skin. Excessive active glucocorticoid (GC) deteriorates skin barrier function...

      Background: 11β-hydroxysteroid dehydrogenase type 1 (11β-HSD1) converts inactive cortisone into cortisol, an active form, and is expressed by several tissues including the skin. Excessive active glucocorticoid (GC) deteriorates skin barrier function.
      Objectives: To find out if 11β-HSD1 affects on the barrier function in aged skin.
      Methods: We have performed human and in vivo studies. We measured cortisol in stratum corneum (SC) and oral epithelium of the elderly and young. Hairless mice were used for 11β-HSD1 immunohistochemistry staining of skin and measuring skin barrier function and serum cytokines. 11β-HSD1 knock-out (KO) mice and its wild-type were used for measuring lipid synthesis related enzyme.
      Results: Cortisol levels were elevated in SC and oral epithelium of the elderly rather than young. The 11β -HSD1 expression was increased in immunohistochemistry stain of aged mice skin. Aged mice showed decreased transepidermal water loss (TEWL) and SC hydration, and increased SC integrity than young. Serum inflammatory cytokines including interleukin-1α, -4, -10, -31 and tumor necrosis factor-α were increased in aged mice than young. The expressions of lipid synthesis related enzymes in epidermis were elevated in KO mice and topical 11β -HSD1 inhibitor applied mice.
      Conclusion: 11β-HSD1 expression is elevated in aged skin. It increases active GC and then deteriorates skin barrier function.

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