Superinduction of mouse epidermal ornithine decarboxylase activity by repeated 12-o-tetradecanoylphorbol-13-acetate treatments.
Superinduction of mouse epidermal ornithine decarboxylase activity by repeated 12-o-tetradecanoylphorbol-13-acetate treatments.
复制标题
通过重复 12-o-十四烷酰佛波醇-13-乙酸酯处理来超诱导小鼠表皮鸟氨酸脱羧酶活性。
DOI：
10.1007/bf00229311
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发表时间：
1996
影响因子：
4.3
通讯作者：
Hayashi,H
中科院分区：
文献类型：
--
作者：
Verma,AK;Hsiao,KM;Ahrens,H;Suganuma,M;Fujiki,H;Matsufuji,S;Hayashi,H
研究了小鼠皮肤表皮蛋白激酶C(PKC)同工酶、鸟氨酸脱羧酶(ODC)mRNA稳态水平和ODC抗酶活性与重复12-O-十四烷基佛波醇-13-乙酸酯(TPA)诱导小鼠皮肤鸟氨酸脱羧酶(ODC)活性的相关性。在CD-1雌性小鼠皮肤上单独应用TPA可显著诱导ODC活性(≈为3nmolCO_2/60min/mg蛋白质)，在处理后约5h达到高峰。然而，在第一次TPA处理后48或72小时，第二次施加TPA时，观察到ODC活性的超级诱导(≈13CO2/60min/mg蛋白)。预先在小鼠皮肤上应用肿瘤起始量的7，12-二甲基苯并[a]蒽并不影响重复TPA治疗引起ODC的程度。用蛋白激酶Cα，β，γ，ɛ和S的抗体进行的Western Blot分析表明，在小鼠表皮提取物中可以检测到蛋白激酶Cα，β，δ和ε的水平。单次局部应用20nmolTPA对小鼠皮肤的影响的时间进程表明，在TPA过度诱导ODC的时间段(72h)，没有一种蛋白激酶C同工酶(α，β，γ，δ和ɛ)完全下调。TPA诱导的ODC mRNA的稳态水平与TPA过度诱导ODC活性的程度无关。第二次TPA处理在第一次TPA处理后72h，导致ODC活性的超诱导，但并未降低ODC-抗酶水平。结果表明，小鼠表皮ODC活性的超诱导部分是转录后调节的，可能不是PKC亚型(S)的丢失或ODC抗酶水平的降低所致。
A correlation of the levels of epidermal protein kinase C (PKC) isozymes, steady state levels of ornithine decarboxylase (ODC) mRNA, and ODC antizyme with the induction of ornithine decarboxylase (ODC) activity by a second repeat 12-O-tetradecanoylphorbol-13-acetate (TPA) treatment to mouse skin was determined. A single application of TPA to female CD-1 mouse skin leads to a dramatic induction of ODC activity (≈3 nmol CO2/60 min/mg protein) which peaks at about 5 h after treatment. However, a superinduction of ODC activity (≈13 CO2/60 min/mg protein) is observed upon the second TPA application at 48 or 72 h after the first TPA treatment. Prior application of a tumor initiating dose of 7,12-dimethylbenz[a]anthracine to mouse skin did not influence the degree of induction of ODC by a repeat TPA treatment. Western Blot analyses using antibodies specific to PKC α, β, γ, ɛ and s indicate detectable levels of PKC α, β, δ and ε in mouse epidermal extracts. A time course of the effects of a single topical application of 20 nmol of TPA to the mouse skin indicate that none of PKC isozymes (α, β, γ, δ and ɛ) were completely downregulated at times (72 h) when ODC was overinduced by TPA. TPA-induced steady state levels of ODC mRNA did not correlate with the degree of superinduction of ODC activity by TPA. The second TPA treatment, 72 h after the first TPA treatment, which leads to superinduction of ODC activity did not decrease the levels of the ODC-antizyme. The results indicate that superinduction of mouse epidermal ODC activity is regulated in part post-transcriptionally and may not be the result of either a loss of PKC isoform(s) or a decrease in the levels of ODC antizyme.