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首页> 外文期刊>American Journal of Physiology >Oxygen alters caveolin-1 and nitric oxide synthase-3 functions in ovine fetal and neonatal lung microvascular endothelial cells.
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Oxygen alters caveolin-1 and nitric oxide synthase-3 functions in ovine fetal and neonatal lung microvascular endothelial cells.

机译：氧会改变绵羊胎儿和新生儿肺微血管内皮细胞中的小窝蛋白1和一氧化氮合酶3的功能。

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摘要

We determined the effect of oxygen [approximately 100 Torr (normoxia) and approximately 30-40 Torr (hypoxia)] on functions of endothelial nitric oxide (NO) synthase (NOS-3) and its negative regulator caveolin-1 in ovine fetal and neonatal lung microvascular endothelial cells (MVECs). Fetal NOS-3 activity, measured as NO production with 0.5-0.9 microM 4-amino-5-methylamino-2,7-difluorofluorescein, was decreased in hypoxia by 14.4% (P < 0.01), inhibitable by the NOS inhibitor N-nitro-L-arginine, and dependent on extracellular arginine. Caveolar function, assessed as FITC-BSA (160 microg/ml) endocytosis, was decreased in hypoxia by 13.5% in fetal and 22.8% in neonatal MVECs (P < 0.01). NOS-3 and caveolin-1 were physically associated, as demonstrated by coimmunoprecipitation and colocalization, and functionally associated, as shown by cross-activation of endocytosis, by their specific antibodies and activation of NOS by albumin. Caveolin peptide, containing the sequence for the PKC phosphorylation site of caveolin, and caveolin antiserum against the site increased NO production and endocytosis by 12.3% (P < 0.05) and 16% (P < 0.05), respectively, in normoxia and increased endocytosis by 25% (P < 0.001) in hypoxia. PMA decreased NO production in normoxia and hypoxia by 19.32% (P < 0.001) and 11.8% (P < 0.001) and decreased endocytosis in normoxia by 20.35% (P < 0.001). PKC kinase activity was oxygen sensitive, and threonine phosphorylation was enhanced in hypoxia. Pertussis toxin increased caveolar and NOS functions. These data support our hypothesis that increased Po(2) at birth promotes dissociation of caveolin-1 and NOS-3, with an increase in their activities, and that PKC and an oxygen-sensitive cell surface G protein-coupled receptor regulate caveolin-1 and NOS-3 interactions in fetal and neonatal lung MVECs.
机译：我们确定了氧气[约100 Torr（正常氧）和约30-40 Torr（低氧）]对绵羊胎儿和新生儿内皮一氧化氮（NO）合酶（NOS-3）及其负调节因子小窝蛋白1的作用。肺微血管内皮细胞（MVEC）。胎儿NOS-3活性（以0.5-0.9 microM 4-氨基-5-甲基氨基-2,7-二氟荧光素产生的NO来衡量）在缺氧状态下降低了14.4％（P <0.01），可被NOS抑制剂N-硝基抑制-L-精氨酸，并依赖于细胞外的精氨酸。缺氧情况下，评估为FITC-BSA（160微克/毫升）胞吞的海绵体功能在胎儿中降低了13.5％，在新生儿MVEC中降低了22.8％（P <0.01）。如通过共免疫沉淀和共定位所证明，NOS-3和小窝蛋白-1在物理上相关，而通过内吞作用的交叉激活，其特异性抗体和白蛋白对NOS的激活，在功能上相关。在正常氧水平下，含有小窝蛋白PKC磷酸化位点序列的小窝蛋白肽和针对该位点的小窝蛋白抗血清分别使NO生成和内吞增加了12.3％（P <0.05）和16％（P <0.05），并增加了内吞作用。缺氧率为25％（P <0.001）。 PMA在常氧和低氧状态下减少NO生成量分别为19.32％（P <0.001）和11.8％（P <0.001），并在常氧下减少内吞作用20.35％（P <0.001）。缺氧时PKC激酶活性对氧敏感，苏氨酸磷酸化增强。百日咳毒素增加了小窝和NOS功能。这些数据支持我们的假设，即出生时Po（2）的增加会促进小窝蛋白1和NOS-3的解离，并增加它们的活性，并且PKC和氧敏感性细胞表面G蛋白偶联受体调节小窝蛋白1和胎儿和新生儿肺MVEC中的NOS-3相互作用。

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