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首页> 外文期刊>American Journal of Physiology >Podokinesis in endothelial cell migration: role of nitric oxide.
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Podokinesis in endothelial cell migration: role of nitric oxide.

机译：Podokinesis在内皮细胞迁移中的作用：一氧化氮的作用。

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Previously, we demonstrated the role of nitric oxide (NO) in transforming epithelial cells from a stationary to locomoting phenotype [E. Noiri, T. Peresleni, N. Srivastava, P. Weber, W.F. Bahou, N. Peunova, and M. S. Goligorsky. Am. J. Physiol. 270 (Cell Physiol. 39): C794-C802, 1996] and its permissive function in endothelin-1-stimulated endothelial cell migration (E. Noiri, Y. Hu, W. F. Bahou; C. Keese, I. Giaever, and M. S. Goligorsky, J. Biol: Chem. 272: 1747-1753, 1997). In the present study, the role of functional NO synthase in executing the vascular endothelial growth factor (VEGF)-guided program of endothelial cell migration and angiogenesis was studied in two independent experimental settings. First, VEGF, shown to stimulate NO release from simian virus 40-immortalized microvascular endothelial cells, induced endothelial cell transwell migration, whereas NG-nitro-L-arginine methyl ester (L-NAME) or antisense oligonucleotides to endothelial NO synthase suppressed this effect of VEGF. Second, in a series of experiments on endothelial cell wound healing, the rate of VEGF-stimulated cell migration was significantly blunted by the inhibition of NO synthesis. To gain insight into the possible mode of NO action, we next addressed the possibility that NO modulates cell matrix adhesion by performing impedance analysis of endothelial cell monolayers subjected to NO. The data showed the presence of spontaneous fluctuations of the resistance in ostensibly stationary endothelial cells. Spontaneous oscillations were induced by NO, which also inhibited cell matrix adhesion. This process we propose to term "podokinesis" to emphasize a scalar from of micromotion that, in the presence of guidance cues, e.g., VEGF, is transformed to a vectorial movement. In conclusion, execution of the program for directional endothelial cell migration requires two coexisting messages: NO-induced podokinesis (scalar motion) and guidance cues, e.g., VEGF, which imparts a vectorial component to the movement. Such a requirement for the dual signaling may explain a mismatch in the demand and supply with newly formed vessels in different pathological states accompanied by the inhibition of NO synthase.
机译：以前，我们证明了一氧化氮（NO）在将上皮细胞从静止表型转变为运动型[E. Noiri，T.Peresleni，N.Srivastava，P.Weber，W.F. Bahou，N。Peunova和M.S. Goligorsky。上午。 J.生理学。 270（Cell Physiol。39：C794-C802，1996）及其在内皮素1刺激的内皮细胞迁移中的允许功能（E. Noiri，Y。Hu，WF Bahou; C。Keese，I。Giaever和MS Goligorsky ，J.Biol：Chem.272：1747-1753，1997）。在本研究中，在两个独立的实验环境中研究了功能性NO合酶在执行血管内皮生长因子（VEGF）指导的内皮细胞迁移和血管生成程序中的作用。首先，VEGF刺激猿猴病毒40永生化微血管内皮细胞释放NO，诱导内皮细胞跨孔迁移，而NG-硝基-L-精氨酸甲酯（L-NAME）或内皮NO合酶的反义寡核苷酸抑制了这一作用。 VEGF。第二，在一系列关于内皮细胞伤口愈合的实验中，通过抑制NO的合成，VEGF刺激的细胞迁移的速率明显降低。为了深入了解NO作用的可能模式，我们接下来通过对经历过NO的内皮细胞单层进行阻抗分析来探讨NO调节细胞基质粘附的可能性。数据表明在表面上固定的内皮细胞中存在抗性的自发波动。 NO引起自发振荡，这也抑制了细胞基质的粘附。我们建议将该过程称为“ podokinesis”，以强调微运动的标量，该微运动在存在指导信号（例如VEGF）的情况下转变为矢量运动。总之，执行定向内皮细胞迁移程序需要两种共存的信息：NO诱导的足动蛋白（标量运动）和引导提示（例如VEGF），为运动提供矢量成分。对双重信号转导的这种要求可以解释与处于不同病理状态的新形成的血管的需求和供应不匹配，同时伴随着对NO合酶的抑制。

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