Niemann A, Björklund A, Eizirik D L
Department of Medical Cell Biology, Uppsala University, Sweden.
Mol Cell Endocrinol. 1994 Dec;106(1-2):151-5. doi: 10.1016/0303-7207(94)90197-x.
Nitric oxide, a radical generated by the enzyme nitric oxide synthase (iNOS), may be an important mediator of beta-cell damage in early insulin-dependent diabetes mellitus. We have investigated the molecular regulation of iNOS in insulin-producing RINm5F cells. The data obtained suggest that iNOS is maximally induced in these cells by a 6-h exposure to IL-1 beta or TNF-alpha + IFN-gamma, but not by endotoxin. iNOS mRNA degradation is rapid and it is not affected by IL-1 beta. Interestingly, NO seems to induce a negative feedback on iNOS expression, probably by decreasing iNOS transcription.
一氧化氮是由一氧化氮合酶（诱导型一氧化氮合酶，iNOS）产生的一种自由基，可能是早期胰岛素依赖型糖尿病中β细胞损伤的重要介质。我们研究了胰岛素分泌型RINm5F细胞中iNOS的分子调控。获得的数据表明，这些细胞经6小时暴露于IL-1β或TNF-α + IFN-γ后iNOS被最大程度诱导，但内毒素不会。iNOS mRNA降解迅速且不受IL-1β影响。有趣的是，NO似乎对iNOS表达产生负反馈，可能是通过降低iNOS转录来实现的。
