Abstract
ICAM-1 protein in keratinocytes is thought to contribute to cutaneous inflammatory reactions. Its induction depends—among others—on cytokines such as TNF-α, IFN-γ, IL-1 or on retinoic acid (RA), a key regulator of epidermal homeostasis. We investigated the effect of treatments with TNF-α, RA or their combination on ICAM-1 expression on proliferative or differentiating keratinocytes over an 8 day culture period. Basal ICAM-1 levels were undetectable at low (30 μM) and standard (88 μM) Ca2+and RA alone did not induce ICAM-1. However, at high Ca2+(1500 μM), ICAM-1 levels were augmented in response to RA-treatment. TNF-α induced a transient ICAM-1 increase in NHK, which reached peak-levels 2-4 days post cytokine stimulus. RA potentiated the TNF-α-induced ICAM-1 response in all Ca2+-concentrations. This potentiating effect of RA was confirmed at the mRNA level. In summary, our results establish retinoic acid as an enhancer of TNF-α-induced ICAM-1 levels in NHK.
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