Bigdeli N, Niemann A, Sandler S, Eizirik D L
Department of Medical Cell Biology, Uppsala University, Sweden.
Biochem Biophys Res Commun. 1994 Sep 30;203(3):1542-7. doi: 10.1006/bbrc.1994.2361.
We presently investigated the induction of manganese superoxide dismutase (MnSOD) and nitric oxide synthase (iNOS) mRNA by interleukin-1 beta (IL-1 beta) in insulin-producing RINm5F cells. IL-1 beta induced both mRNAs in parallel, with increased levels detectable after 4 h and further increase at 6 h. Aminoguanidine, a blocker of NO production, did not prevent IL-1 beta-induced MnSOD mRNA expression, and SNP, a NO releasing agent, did not induce MnSOD mRNA. Actinomycin D, an inhibitor of gene transcription, prevented IL-1 beta induction of both MnSOD and iNOS mRNA. Cycloheximide, an inhibitor of protein synthesis, prevented IL-1 beta-induced expression of iNOS mRNA, but not MnSOD mRNA. These data suggest that induction of MnSOD mRNA by IL-1 beta is independent of iNOS expression and NO production. Moreover, while expression of iNOS mRNA depends on protein synthesis, MnSOD mRNA induction does not necessarily require this step. Thus, it seems that IL-1 induces genes potentially involved in cell damage (iNOS) and defense (MnSOD) by different mechanisms.
我们目前研究了白细胞介素-1β（IL-1β）在胰岛素分泌型RINm5F细胞中对锰超氧化物歧化酶（MnSOD）和一氧化氮合酶（iNOS）mRNA的诱导作用。IL-1β同时诱导这两种mRNA，4小时后可检测到水平升高，6小时时进一步升高。氨基胍是一种NO产生的阻滞剂，它不能阻止IL-1β诱导的MnSOD mRNA表达，而SNP是一种NO释放剂，它不能诱导MnSOD mRNA。放线菌素D是一种基因转录抑制剂，它能阻止IL-1β对MnSOD和iNOS mRNA的诱导。环己酰亚胺是一种蛋白质合成抑制剂，它能阻止IL-1β诱导的iNOS mRNA表达，但不能阻止MnSOD mRNA表达。这些数据表明，IL-1β对MnSOD mRNA的诱导独立于iNOS表达和NO产生。此外，虽然iNOS mRNA的表达依赖于蛋白质合成，但MnSOD mRNA的诱导不一定需要这一步骤。因此，似乎IL-1通过不同机制诱导可能参与细胞损伤（iNOS）和防御（MnSOD）的基因。
