Abstract
Though a regulatory role for nitric oxide (NO) in diverse cutaneous functions is well known, whether NO impacts permeability homeostasis remains unexplored. Here, we utilized inducible nitric oxide synthase (iNOS) KO mice to explore the role of NO and iNOS in epidermal homeostasis. Although iNOS KO and wild type mice looked grossly similar, iNOS KO mice displayed a significant abnormality in permeability barrier recovery in comparison with wild type mice, and epidermal biophysical properties were comparable between these two groups at baseline. Consistent with delayed barrier recovery, the expression of genes strongly linked to permeability barrier homeostasis, including epidermal lipid synthetic enzymes (HMGCoA reductase, fatty acid synthase, serine palmitoyltransferase), and keratinocyte differentiation marker-related proteins (filaggrin, loricrin and involucrin) was significantly decreased in iNOS KO mice. Pertinently, topical applications of NO upregulated the expression of epidermal mRNA for lipid production and keratinocyte differentiation in parallel with accelerated barrier recovery in iNOS KO mice. Taken together, these results indicate that the generation of NO by epidermal iNOS is crucial for epidermal homeostasis.
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