Beyaert R, Suffys P, Van Roy F, Fiers W
Laboratory of Molecular Biology, State University of Gent, Belgium.
FEBS Lett. 1990 Mar 12;262(1):93-6. doi: 10.1016/0014-5793(90)80161-b.
The role of the phospholipase inhibitor proteins, lipocortin-I and -II, in tumor necrosis factor (TNF)-mediated cytotoxicity against L929 fibrosarcoma cells was investigated. We previously reported that TNF-mediated cytotoxicity was inhibited by dexamethasone (DEX), suggesting an involvement of lipocortins. Now we show that, despite inhibition by DEX of TNF-induced arachidonic acid release, DEX has no effect on the synthesis of these lipocortins. Moreover, TNF itself has no effect on the synthesis and phosphorylation of lipocortin-I and -II. Also there was no difference in expression levels of lipocortin-I and -II between TNF-sensitive and -resistant cells. These data strongly suggest that the protective effect of DEX and other glucocorticoids is not mediated by lipocortins.
研究了磷脂酶抑制蛋白脂皮质素-I和脂皮质素-II在肿瘤坏死因子（TNF）介导的对L929纤维肉瘤细胞的细胞毒性中的作用。我们之前报道过，地塞米松（DEX）可抑制TNF介导的细胞毒性，提示脂皮质素参与其中。现在我们发现，尽管DEX抑制了TNF诱导的花生四烯酸释放，但DEX对这些脂皮质素的合成没有影响。此外，TNF本身对脂皮质素-I和脂皮质素-II的合成及磷酸化也没有影响。而且，在TNF敏感细胞和耐药细胞之间，脂皮质素-I和脂皮质素-II的表达水平没有差异。这些数据有力地表明，DEX和其他糖皮质激素的保护作用不是由脂皮质素介导的。
