Abstract
Recent studies suggest: that the epidermis and pilosebaceous epithelium are important sites of de novo sterol synthesis, and that the rate of cutaneous cholesterol synthesis does not change with alterations in circulating sterol levels. Since cutaneous sterols may be important for permeability barrier function, we studied the effect of experimentally altered barrier function on de novo sterologenesis in the epidermal and dermal layers of the skin. Epidermal sterologenesis appeared to be modulated by the skin's barrier requirements because topical detergent and acetone treatment stimulated de novo synthesis of nonsaponifiable lipids in the epidermis, but not in the dermis. Synthetic activity paralleled both the return of barrier function toward normal and the extent of prior damage to the barrier. Moreover, plastic-wrap occlusion of solvent-treated sites simultaneously corrected both the barrier abnormality and normalized sterol synthesis, further linking increased epidermal sterologenesis to barrier requirements. Whereas topical applications of a variety of other topical lipids did not down-regulate synthesis, epicutaneously applied 25-hydroxycholesterol appeared to diminish synthesis. These results suggest that maintenance of barrier function is one purpose of epidermal de novo nonsaponifiable lipid synthesis, and demonstrate further that, despite a lack of low density lipoprotein receptors, epidermis can regulate its lipid-synthetic apparatus in response to certain specific requirements.
Highlights
Recent studies suggest: I ) that the epidermis and pilosebaceous epithelium are important sites of de novo sterol synthesis, and 2) that the rate of cutaneous cholesterol synthesis does not change with alterations in circulating sterol levels
Since cutaneous sterols may be important for permeability barrier function, we studied the effect of experimentally altered barrier function on de novo sterologenesis in the epidermal and dermal layers of the skin
We have found that epidermal sterologenesis is not affected by the host's vitamin D requirements; instead the permeability barrier requirements of the skin appear to modulate the intensity of epidermal nonsaponifiable lipid synthesis [11]
Summary
Recent studies suggest: I ) that the epidermis and pilosebaceous epithelium are important sites of de novo sterol synthesis, and 2) that the rate of cutaneous cholesterol synthesis does not change with alterations in circulating sterol levels. Epidermal sterologenesis appeared to be modulated by the skin's barrier requirements because topical detergent and acetone treatment stimulated de novo synthesis of nonsaponifiable lipids in the epidermis, but not in the dermis Synthetic activity paralleled both the return of barrier function toward normal and the extent of prior damage to the barrier. Previous studies have shown that the skin is a major site of sterologenesis in both rodents [1,2,3] and primates [4], accounting for u p to 30% of total body sterol synthesis Of this synthetic activity, we reported recently that about 80% was localized to the dermal layer in rodents, presumably emanating from the pilosebaceous epithelium which remained with the dermis [5]. We have found that epidermal sterologenesis is not affected by the host's vitamin D requirements; instead the permeability barrier requirements of the skin appear to modulate the intensity of epidermal nonsaponifiable lipid synthesis [11]
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