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cGMP-dependent and -independent properties of nitric angiogenesis-related oxide

机译：一氧化氮与血管生成相关的cGMP依赖性

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Nitric oxide exerts a stimulatory role during postnatal angiogenesis. Although soluble guanylyl cyclase (sGC) mediates many of the effects of nitric oxide (NO) in the vascular system, the contribution of cGMP-dependent vs cGMP-independent pathways in NO-induced angiogenesis remains unclear. Herein, we determined the effects of a NO donor (sodium nitroprusside; SNP) and a NO-independent sGC activator (BAY 41-2272) in the growth and migration of rat aortic endothelial cells (RAEC). RAEC lack enzymatically active sGC as suggested by their inability to accumulate cGMP upon exposure to SNP. However, treatment of RAEC with SNP promoted a modest increase in their proliferation and migration that was dependent on extracellular signal regulated kinase1/2 activation. Moreover, when RAEC were exposed to vascular endothelial growth factor we observed an increase in migration that was inhibited by NO synthase, but not sGC, inhibition. Infection of cells with adenoviruses containing sGC greatly increased the efficacy of SNP as a mitogenic and migratory stimulus. We conclude that NO is capable of stimulating EC proliferation and mobility in the absence of sGC; however, increased intracellular levels of cGMP following sGC activation greatly amplify the angiogenic potential of NO. (C) 2007 Elsevier Inc. All rights reserved.
机译：一氧化氮在产后血管生成过程中发挥刺激作用。尽管可溶性鸟苷基环化酶（sGC）介导了血管系统中一氧化氮（NO）的许多作用，但尚不清楚cGMP依赖性与cGMP依赖性途径在NO诱导的血管生成中的作用。本文中，我们确定了NO供体（硝普钠; SNP）和NO非依赖性sGC激活剂（BAY 41-2272）对大鼠主动脉内皮细胞（RAEC）生长和迁移的影响。 RAEC缺乏酶活性的sGC，这是由于它们在暴露于SNP后无法累积cGMP所暗示。但是，用SNP治疗RAEC可促进其增殖和迁移的适度增加，这取决于细胞外信号调节的激酶1/2活化。此外，当RAEC暴露于血管内皮生长因子时，我们观察到迁移的增加受到NO合酶的抑制，而不受sGC的抑制。用含有sGC的腺病毒感染细胞大大提高了SNP作为有丝分裂和迁移刺激的功效。我们得出的结论是，在没有sGC的情况下，NO能够刺激EC增殖和迁移。然而，sGC激活后细胞内cGMP水平的增加极大地放大了NO的血管生成潜力。 （C）2007 Elsevier Inc.保留所有权利。

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