Nadaud S, Laumonnier Y, Soubrier F
INSERM U 525, CHU Pitié-Salpêtrière, 91, boulevard de l'hôpital, 75013 Paris.
J Soc Biol. 2000;194(3-4):131-5.
The endothelial isoform of nitric oxide synthase (eNOS) ensures enzymatic production of nitric oxide (NO) not only in endothelial cells but also in other cell types, such as neurons, platelets, and some epithelial cells. Its physiological role has been well defined in some of these cells, such as relaxation of vascular smooth muscle cells, or long-term potentiation in neurons, owing to knockout experiments. Although constitutively expressed in endothelial cells, eNOS mRNA has been shown to be modulated by several physical, biochemical, and hormonal factors, acting at the transcriptional or post-transcriptional levels. Several functional regulatory elements have been mapped in the eNOS promoter, active both in endothelial and non-endothelial cells, and we present elements demonstrating that these elements are not sufficient to explain the high level of eNOS expression specific to endothelial cells.
一氧化氮合酶（eNOS）的内皮亚型不仅在内皮细胞中，而且在其他细胞类型中，如神经元、血小板和一些上皮细胞中，确保一氧化氮（NO）的酶促生成。由于基因敲除实验，其生理作用在其中一些细胞中已得到很好的定义，如血管平滑肌细胞的舒张或神经元的长期增强。尽管eNOS mRNA在内皮细胞中组成性表达，但已表明它受到几种物理、生化和激素因素的调节，这些因素在转录或转录后水平起作用。在eNOS启动子中已定位了几个功能调节元件，它们在内皮细胞和非内皮细胞中均有活性，并且我们展示的元件表明这些元件不足以解释内皮细胞特有的eNOS高表达水平。
