Cytokine-induced expression of a nitric oxide synthase in rat renal tubule cells.
Cytokine-induced expression of a nitric oxide synthase in rat renal tubule cells.
复制标题
DOI：
10.1172/jci116439
复制
发表时间：
1993-05
期刊：
影响因子：
--
通讯作者：
B. Markewitz;J. Michael;D. Kohan
中科院分区：
文献类型：
--
作者：
B. Markewitz;J. Michael;D. Kohan
一氧化氮（NO.）与肾血管张力和肾小管钠转运的调节有关。虽然内皮细胞是众所周知的NO（.）来源，最近的研究表明，肾小管上皮细胞可以组成性地产生NO（.）。一氧化氮合酶的一种诱导型亚型，在某些细胞类型中产生大量的NO。我们试图确定是否肾上皮细胞暴露于细胞因子可以表达诱导型一氧化氮合酶。原代培养的大鼠近曲小管和内髓集合管细胞在暴露于TNF-α和IFN-γ时产生NO。NO.生产由这两种细胞类型的抑制NG-单甲基-L-精氨酸，这种抑制作用部分逆转了过量的L-精氨酸的加入。用TNF-α和IFN-γ刺激肾上皮细胞显著增加诱导型一氧化氮合酶mRNA的水平。总之，肾近端小管和内髓集合管细胞可以通过表达一氧化氮合酶的诱导型亚型产生NO。
Nitric oxide (NO.) has been implicated in the regulation of renal vascular tone and tubular sodium transport. While the endothelial cell is a well known source of NO(.), recent studies suggest that tubular epithelial cells may constitutively generate NO(.). An inducible isoform of nitric oxide synthase which produces far greater quantities of NO. exists in some cell types. We sought to determine whether kidney epithelial cells exposed to cytokines could express an inducible nitric oxide synthase. Primary cultures of rat proximal tubule and inner medullary collecting duct cells generated NO. on exposure to TNF-alpha and IFN-gamma. NO. production by both cell types was inhibited by NG-monomethyl-L-arginine; this inhibition was partially reversed by the addition of excess L-arginine. Stimulation of kidney epithelial cells with TNF-alpha and IFN-gamma dramatically increased the level of inducible nitric oxide synthase mRNA. In summary, renal proximal tubule and inner medullary collecting duct cells can produce NO. via expression of an inducible isoform of nitric oxide synthase.