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Protein kinase C isoform levels in normal and sodium dodecyl sulphate‐irritated mouse skin
Author(s) -
Li Lf,
Fiedler Vc,
Raj Kumar
Publication year - 1998
Publication title -
british journal of dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.304
H-Index - 179
eISSN - 1365-2133
pISSN - 0007-0963
DOI - 10.1046/j.1365-2133.1998.02306.x
Subject(s) - protein kinase c , gene isoform , kinase , threonine , chemistry , serine , sodium dodecyl sulfate , microbiology and biotechnology , protein kinase a , signal transduction , biochemistry , phosphorylation , biology , gene
Protein kinase C (PKC) comprises a family of related phospholipid‐dependent serine/threonine protein kinases. PKC is important in signal transduction, regulating cell proliferation and differentiation. Recently, it has also been suggested that PKC may play a part in the pathogenesis of contact dermatitis. However, the expression of PKC isoforms in the skin of mice with irritant contact dermatitis (ICD) has not been examined. In this study, ICD was induced in mouse skin by applying 5%, 10% and 20% sodium dodecyl sulphate (SDS) in Finn chambers on the backs of mice and fixing with surgical dressings for 24 h. Depending upon the SDS concentration, mild to strong skin irritant reactions were observed 24 h after removal of the irritant patches. The intensity of the reactions increased with the increasing concentration of SDS. PKC isoforms α, β, γ and δ were all detected in normal mouse skin by Western immunoblotting. The specificity of the PKC isoforms detected was identified further by competitive Western immunoblotting. Compared with normal mouse skin treated with double‐distilled water, the levels of PKC isoforms α, β, γ and δ in the SDS‐irritated mouse skin was decreased by 24.8–75.8%. These results suggest that, in SDS‐ICD, mouse skin PKC isoforms α, β, γ and δ are down‐regulated. The significance of this decrease is under further investigation.