Comparative Evaluation of TRAIL, FGF-2 and VEGF-A-Induced Angiogenesis In Vitro and In Vivo.
Comparative Evaluation of TRAIL, FGF-2 and VEGF-A-Induced Angiogenesis In Vitro and In Vivo.
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DOI：
10.3390/ijms17122025
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发表时间：
2016-12-02
影响因子：
5.6
通讯作者：
Kavurma MM
中科院分区：
文献类型：
--
作者：
Cartland SP;Genner SW;Zahoor A;Kavurma MM
肿瘤坏死因子相关的凋亡诱导配体(TRAIL)与血管生成有关，即从现有的血管床生长新的血管。我们的目的是比较TRAIL、血管内皮生长因子-A(VEGF-A)和成纤维细胞生长因子-2(成纤维细胞生长因子-2)单独或联合使用时的促血管生成反应，然后评估体外培养的人微血管内皮细胞(HMEC-1)的增殖、迁移和小管形成。体内血管生成也使用Matrigel Plug实验进行测量。TRAIL和成纤维细胞生长因子-2显著促进HMEC-1细胞的增殖和迁移，联合治疗仅对细胞迁移有增强作用。相反，10 ng/mLVEGF-A不能刺激HMEC-1的迁移。三种因素均可诱导肾小管形成，TRAIL较血管内皮生长因子-A更有效，但不能诱导成纤维细胞生长因子-2。400 ng/mLTRAIL可促进CD31阳性染色进入Matrigel栓，但对VEGF-A无作用。但在体内，成纤维细胞生长因子-2在促进细胞浸润和血管生成方面优于TRAIL和VEGF-A。这些发现表明，在体外和体内，每种生长因子在不同的血管生成过程中都更有效。了解这些分子如何刺激与血管生成相关的不同过程，可能有助于确定旨在抑制或促进人类失调的血管生成的新策略和治疗方法。
Tumor necrosis-factor-related apoptosis-inducing ligand (TRAIL) has been implicated in angiogenesis; the growth of new blood vessels from an existing vessel bed. Our aim was to compare pro-angiogenic responses of TRAIL, vascular endothelial growth-factor-A (VEGF-A) and fibroblast growth-factor-2 (FGF-2) either separately (10 ng/mL) or in combination, followed by the assessment of proliferation, migration and tubule formation using human microvascular endothelial-1 (HMEC-1) cells in vitro. Angiogenesis was also measured in vivo using the Matrigel plug assay. TRAIL and FGF-2 significantly augmented HMEC-1 cell proliferation and migration, with combination treatment having an enhanced effect on cell migration only. In contrast, VEGF-A did not stimulate HMEC-1 migration at 10 ng/mL. Tubule formation was induced by all three factors, with TRAIL more effective compared to VEGF-A, but not FGF-2. TRAIL at 400 ng/mL, but not VEGF-A, promoted CD31-positive staining into the Matrigel plug. However, FGF-2 was superior, stimulating cell infiltration and angiogenesis better than TRAIL and VEGF-A in vivo. These findings demonstrate that each growth factor is more effective at different processes of angiogenesis in vitro and in vivo. Understanding how these molecules stimulate different processes relating to angiogenesis may help identify new strategies and treatments aimed at inhibiting or promoting dysregulated angiogenesis in people.
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作者：
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通讯作者：
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