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Published on: September 7, 2013
Mice lacking 25OHD 1alpha-hydroxylase demonstrate decreased epidermal differentiation and barrier function
D D Bikle1, S Chang, D Crumrine
1Department of Medicine, Veterans Affairs Medical Center, University of California, 4150 Clement Street (111N), San Francisco, CA 94121, USA. doctor@itsa.ucsf.edu
Summary
Vitamin D is essential for skin barrier function. Mice lacking 1alpha-hydroxylase (1OHase) showed impaired keratinocyte differentiation and delayed skin barrier repair, highlighting the role of 1,25(OH)(2)D in epidermal health.
Area of Science:
- Dermatology
- Endocrinology
- Cell Biology
Background:
- Keratinocytes express 25OHD 1alpha-hydroxylase (1OHase), producing 1,25(OH)(2)D.
- 1,25(OH)(2)D promotes keratinocyte differentiation in vitro.
Purpose of the Study:
- To determine if 1OHase activity is essential for keratinocyte differentiation in vivo.
- To investigate the role of 1,25(OH)(2)D in epidermal barrier formation and maintenance.
Main Methods:
- Examined differentiation in 1alphaOHase(-/-) mice using microscopy and immunocytochemistry.
- Assessed calcium localization via ion capture cytochemistry.
- Evaluated barrier integrity using transepidermal water loss (TEWL).
Main Results:
- Reduced levels of differentiation markers (involucrin, filaggrin, loricrin) in 1alphaOHase(-/-) mice.
- Decreased epidermal calcium and loss of calcium gradient.
- Impaired skin barrier recovery after disruption in knockout mice, linked to reduced lamellar body secretion.
Conclusions:
- 1,25(OH)(2)D is crucial for normal epidermal differentiation and barrier function.
- This likely occurs through protein induction and calcium signaling necessary for barrier generation and maintenance.
