SKIN-DERIVED ANTILEUKOPROTEINASE (SKALP) AND EPIDERMAL FATTY-ACID-BINDING PROTEIN (E-FABP) - 2 NOVEL MARKERS OF THE PSORIATIC PHENOTYPE THAT RESPOND DIFFERENTIALLY TO TOPICAL STEROID
Ala. Kuijpers et al., SKIN-DERIVED ANTILEUKOPROTEINASE (SKALP) AND EPIDERMAL FATTY-ACID-BINDING PROTEIN (E-FABP) - 2 NOVEL MARKERS OF THE PSORIATIC PHENOTYPE THAT RESPOND DIFFERENTIALLY TO TOPICAL STEROID, Acta dermato-venereologica, 77(1), 1997, pp. 14-19
Recently we have described two novel markers for disturbed epidermal d
ifferentiation, which are strongly upregulated in psoriatic epidermis:
skin-derived antilenkoproteinase (SKALP) and epidermal fatty acid-bin
ding protein (E-FABP). No data are available on the kinetics of SKALP
and E-FABP expression in vivo and the relation with epidermal growth a
nd differentiation. We used treatment of lesional psoriatic skin with
topical steroid as a model to correlate the expression pattern of SKAL
P and E-FABP with known cell biological events during regression of th
e psoriatic lesion. Expression of these markers was studied using immu
nohistochemistry and Northern blot analysis. After 4 weeks of treatmen
t a substantial clinical improvement was induced by the topical steroi
d, whereas no significant improvement had occurred at the placebo-trea
ted sides. The expression of SKALP following treatment with steroid wa
s nearly undetectable both at the protein and mRNA level. Mitotic acti
vity, as measured by Ki-67 staining, and cytokeratin 16 expression wer
e downregulated to normal levels in the steroid-treated epidermis. In
contrast, although there was a marked decrease of E-FABP mRNA, the sta
ining pattern for E-FABP at the protein level was not affected. After
4 weeks of treatment with steroid the complete suprabasal compartment
remained positive, even after considerable clinical improvement of the
lesion. We conclude that SKALP and cytokeratin 16 are markers that ar
e downregulated even before complete macroscopic clearance of the lesi
on. The kinetics of E-FABP expression is distinct from the other molec
ules and lags behind the clinical signs of psoriasis.