Corticotropin-releasing hormone stimulates NF-κB in human epidermal keratinocytes

Corticotropin-releasing hormone (CRH) has been shown to inhibit proliferation and modulate expression of inflammation markers in the epidermal cells. In the present study we report that CKH also stimulates nuclear factor-kappa B (NF-kappaB) activity. Incubation with CRH of human keratinocytes derived front primary cultures resulted in increased binding of DNA by NF-kappaB. CRH induced translocation of NF-kappaB subunit p65 front the cytoplasm to the nucleus and induced expression of kappaB-driven chloramphenicol acetyltransferase (CAT) reporter gene. NF-kappaB translocation was accompanied by degradation of the inhibitor of NF-kappaB a (IkappaB-alpha). Specificity of the CRH effect was demonstrated by the use of CRH-R antagonists antalarmin and a-helical CRH [9-41]. CRH-dependent stimulation of NF-kappaB activity is consistent with accumulated data about role of this neuropeptide in the regulation of local epidermal homeostasis.