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首页> 外文期刊>Circulation journal >Urotensin II Stimulates Vascular Endothelial Growth Factor Secretion From Adventitial Fibroblasts in Synergy With Angiotensin II
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Urotensin II Stimulates Vascular Endothelial Growth Factor Secretion From Adventitial Fibroblasts in Synergy With Angiotensin II

机译：Urotensin II与血管紧张素II协同刺激从成纤维细胞刺激血管内皮生长因子分泌

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Background: The adventitia plays an important role in and is considered to be the initiating site for vascular remodeling. Urotensin II (UII) and angiotensin II (Ang II) are the two most important vascular peptides involved in vascular remodeling in the adventitia. Nevertheless, little is known about their effect on the expression of vascular endothelial growth factor (VEGF). It was hypothesized that both UII and Ang II could induce VEGF expression in adventitial fibroblasts and VEGF may play a role in cell proliferation and collagen I synthesis induced by UII or Ang II. Methods and Results: Growth-arrested adventitial fibroblasts were incubated in serum-free medium with UII and/or Ang II and inhibitors of the mitogen-activated protein kinase (MAPK) pathway or VEGF-neutralizing antibodies. The VEGF expression was evaluated using enzyme-linked immunosorbent assay (ELISA), while the proliferation and collagen I synthesis were detected using methyl thiazol tetrazolium (MTT) assay and ELISA. It was found that: (1) both UII and Ang II could stimulate VEGF expression in adventitial fibroblasts and they had a synergistic effect; (2) MAPK pathway inhibitors could inhibit VEGF secretion induced by UII and/or Ang II; and (3) VEGF-neutralizing antibodies could inhibit UII/Ang II-induced cell proliferation and collagen synthesis in adventitial fibroblasts. Conclusions: Induction of VEGF expression may be a new mechanism involved in vascular remodeling for UII and Ang II. ( Circ J 2012; 76: 1267-1273)
机译：背景：外膜在血管重构中起着重要作用，被认为是血管重构的起始部位。血管紧张素II（UII）和血管紧张素II（Ang II）是外膜中涉及血管重构的两个最重要的血管肽。然而，关于它们对血管内皮生长因子（VEGF）表达的影响知之甚少。假设UII和Ang II均可以诱导外膜成纤维细胞中的VEGF表达，并且VEGF可能在UII或Ang II诱导的细胞增殖和胶原I合成中起作用。方法和结果：将生长停滞的外膜成纤维细胞在无血清培养基中与UII和/或Ang II以及有丝分裂原激活的蛋白激酶（MAPK）通路抑制剂或VEGF中和抗体一起孵育。使用酶联免疫吸附测定（ELISA）评估VEGF表达，同时使用甲基噻唑四唑（MTT）测定和ELISA检测增殖和胶原I合成。发现：（1）UII和Ang II均能刺激外膜成纤维细胞中的VEGF表达，并具有协同作用; （2）MAPK途径抑制剂可抑制UII和/或Ang II诱导的VEGF分泌; （3）VEGF中和抗体可以抑制UII / Ang II诱导的外膜成纤维细胞增殖和胶原合成。结论：诱导VEGF表达可能是UII和Ang II血管重构的新机制。 （Circ J 2012; 76：1267-1273）

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