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  • 1
    Electronic Resource
    Electronic Resource
    Copenhagen : Munksgaard International Publishers
    Experimental dermatology 9 (2000), S. 0 
    ISSN: 1600-0625
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract: Nitric oxide (NO), which has several physiological functions in skin, is generated by NO synthase (NOS). NOS has at least three isoforms; endothelial NOS (eNOS), brain NOS (bNOS), and inducible NOS (iNOS). Ultraviolet B (UVB) irradiation has been reported to stimulate NO production in skin via induction or activation of NOS, however, the exact mechanism of NOS induction by UVB irradiation remains obscure. In this study, we investigated the direct effect of UVB on the expression of NOS isoforms in murine keratinocytes, and found a significant increase in NO production within 48 h. mRNA and protein expressions of bNOS were both enhanced by UVB irradiation in murine keratinocytes, whereas iNOS mRNA expression was suppressed at 4 and 12 h after UVB irradiation. These results suggest that the enhancement of NO production observed after UVB irradiation in murine keratinocytes may be explained in part by the upregulation of bNOS expression, but not iNOS expression.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-069X
    Keywords: Key words Ultraviolet B radiation ; Nitric oxide ; Nitric oxide synthase ; Murine keratinocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract  Ultraviolet radiation causes inflammation characterized by erythema and swelling, but also exhibits antiinflammatory effects which have led to the use of ultraviolet B radiation (UVBR) and psoralen plus ultraviolet A (PUVA) in the treatment of psoriasis, chronic severe atopic dermatitis and uremic pruritus. In inflammatory dermatoses, a pathogenic role of nitric oxide (NO) derived from inducible nitric oxide synthase (iNOS) has been suggested. To elucidate how UVBR regulates iNOS expression in skin under inflammatory conditions, we investigated the effect of UVBR on NO production and iNOS expression in cultured murine keratinocyte Pam 212 cells stimulated with interferon-Á (IFN-Á) or tumor necrosis factor-· (TNF-·). Low doses of UVBR significantly suppressed IFN-Á- or TNF-·-induced NO production. UVBR also downregulated IFN-Á- or TNF-·-induced iNOS expression at both the mRNA level and the protein level. These findings suggest the possibility that the downregulatory effect of UVBR on IFN-Á- or TNF-·-induced iNOS expression may, in part, explain the antiinflammatory and therapeutic properties of UVBR in inflammatory dermatoses.
    Type of Medium: Electronic Resource
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