Scott-Burden T, Elizondo E, Ge T, Boulanger C M, Vanhoutte P M
Center for Experimental Therapeutics, Baylor College of Medicine, Houston, TX 77030.
Biochem Biophys Res Commun. 1993 Nov 15;196(3):1261-6. doi: 10.1006/bbrc.1993.2388.
Induction of NO synthase expression by interleukin-1 beta in cultured vascular smooth muscle cells from rat aortas was accompanied by simultaneous induction of GTP: cyclohydrolase I. This enzyme regulates the de novo synthesis pathway for tetrahydrobiopterin, an essential cofactor for the catalytic conversion of L-arginine to L-citrulline and NO by inducible NO synthase. Inhibition of GTP: cyclohydrolase attenuated NO production by interleukin-1 beta-stimulated smooth muscle cells. Peptide growth factors such as fibroblast growth factor, platelet-derived growth factor and transforming growth factor beta 1 and the protease thrombin have been shown to modulate the production NO by cytokine-treated smooth muscle cells. These peptide agonists also regulated the induction of NO synthase and GTP: cyclohydrolase mRNA expression.
白细胞介素-1β在大鼠主动脉培养的血管平滑肌细胞中诱导一氧化氮合酶表达的同时，还诱导了鸟苷三磷酸环化水解酶I的表达。该酶调节四氢生物蝶呤的从头合成途径，四氢生物蝶呤是诱导型一氧化氮合酶将L-精氨酸催化转化为L-瓜氨酸和一氧化氮所必需的辅助因子。抑制鸟苷三磷酸环化水解酶可减弱白细胞介素-1β刺激的平滑肌细胞产生一氧化氮。已表明，诸如成纤维细胞生长因子、血小板衍生生长因子和转化生长因子β1等肽生长因子以及蛋白酶凝血酶可调节细胞因子处理的平滑肌细胞产生一氧化氮。这些肽激动剂还调节一氧化氮合酶的诱导和鸟苷三磷酸环化水解酶mRNA的表达。
