Fatty acid binding proteins

Abstract

Repeated exposure of the skin to irritants may lead to stratum corneum disruption and chronic irritant contact dermatitis. Impairment of the barrier function and damage to epidermal cells are followed by barrier repair and enhanced epidermal lipid metabolism. Barrier perturbation regulates epidermal mRNA levels for the rate-limiting enzymes of ceramide, sterol, and free fatty acid synthesis [13]. Studies in humans have indicated that exposure to specific irritants can lead to specific cutaneous reactions depending on the nature of the chemical [39]. Noting only erythema and an increase of transepidermal water loss (TEWL) after application of sodium dodecyl sulfate (SDS), the biological response of keratinocytes to barrier perturbation was shown to include: 1. An increased proliferative rate 2. The induction of involucrin 3. The induction of a cytosolic fatty acid binding protein (FABP) [17] Induction of involucrin may indicate stimulated differentiation of the proteinaceous part of the epidermal barrier. Induction of the epidermal FABP might reflect the temporary increase in lipid traffic associated with abnormal keratinocyte differentiation. Required is a better understanding of the complex mechanisms by which fatty acids (FA) are taken up and distributed in the keratinocyte under stress, i.e., irritancy to the epidermal barrier. Therefore, an overview of the current understanding of FA metabolism, intracellular FA transport, and cellular FA uptake is given with respect to the epidermal barrier. © 2006 Springer-Verlag Berlin Heidelberg.