Protein kinase C isoform levels in normal and sodium dodecyl sulphate-irritated mouse skin

Abstract

p53 plays an essential part in the maintenance of the cellular genetic stability after a DNA-damaging event such as ultraviolet (UV) radiation. Following UV radiation, the amount of p53 protein is elevated. The increased p53 is believed to induce cell cycle arrest, promote nucleotide excision repair (NER) and apoptosis. To study if cells respond differently to high- and low-dose UV radiation, we examined the DNA repair efficiency and apoptosis rate of human and murine fibroblasts after UV radiation. Using a host cell reactivation assay, we found that NER was increased after low doses but not after high doses of UV radiation. In contrast, apoptosis occurred only after the cells received high doses (over 200 J/m2), but not low doses of UVB. The induction of both NER and apoptosis was observed only in p53+/+ murine fibroblasts, not in p53-/- cells, indicating that both stress response mechanisms are dependent on wild-type p53 function. UV radiation induced the expression of p53 protein in a dose-dependent manner up to 400 J/m2. In contrast, p21waf1/cip1 was induced only after low doses and bax only after high doses of UV radiation, supporting the roles of p21waf1/cip1 and bax in NER and apoptosis, respectively. Taken together, these results indicate that cellular stress response to UV radiation depends on UV dose, DNA repair after low doses and apoptosis after high doses, and that both mechanisms are dependent on wild-type p53 function.

Induction of hair growth by skin irritants and its relation to skin protein kinase C isoforms

“…It is known that anthralin is a strong skin irritant and in our study, 0.1% anthralin caused severe dermatitis, quicker elevation of PKC α and earlier hair growth enhancement than 10% SDS (Figs 2 and 3). We have also reported that the degree of change in PKC increases with increasing concentration of SDS 14 . Whether higher concentrations of SDS, which induce more significant PKC changes, may exhibit a better hair growth response in AA, is not known.…”

“…Three mice were used for each time point. As we have reported downregulation of PKC α, β, γ and δ isoforms in SDS‐irritated skin at 24 h after irritation, 14 therefore, skin biopsies were not taken at 1 day after SDS treatment in this study. The biopsies were placed epidermis side down on an ice‐cold Petri dish and subcutaneous tissue was quickly removed with a razor blade and discarded.…”

“…Skin PKC isoforms were detected by Western blot as previously reported by us 14 . Briefly, mouse skin specimens were homogenized in extraction buffer containing 25 mmol/L Tris–HCl (Sigma), 5 mmol/L ethylenediamine tetraacetic acid (Fisher Scientific Company, Fair Lawn, NJ, U.S.A.), 20 mmol/L mercaptoethanol (Sigma), 1 mmol/L phenylmethylsulphonyl fluoride (Sigma), 5% glycerol and 0.5% Triton X‐100 (Sigma), as well as 10 μg/mL pepstatin, leupeptin and aprotinin (Sigma).…”

Oral Intake ofLactobacillus helveticus-Fermented Milk Whey Decreased Transepidermal Water Loss and Prevented the Onset of Sodium Dodecylsulfate-Induced Dermatitis in Mice

“…[10][11][12] Our procedure, a modified version of the method reported by Kawano,13) induced a decrease in skin moisture content, to less than 50% of the level of native skin, and this state persisted for 4 d after the cessation of SDS exposure. Since the differences among the evaluated parameters between the sample group and the control group were found to be significant, our procedure is considered to be appropriate for evaluation of the efficacy of skin care regimens.…”