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Hypoxia and endothelin-1 induce VEGF production in human vascular smooth muscle cells.

机译:缺氧和内皮素-1诱导人血管平滑肌细胞中VEGF的产生。

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摘要

Vascular endothelial growth factor/vascular permeability factor (VEGF/VPF) is a secreted mitogen for vascular endothelial cells, and it promotes vascular permeability and neovascularization in vivo. We investigated the mechanisms by which low oxygen tension modulates the expression of VEGF in human aortic vascular smooth muscle cells (h-SMC) in vitro. Moreover, we measured VEGF levels in the cultured medium with or without endothelin-1 (ET-1) using a newly developed, highly sensitive, enzyme-linked immunosorbent assay. Hypoxia resulted in a substantial induction of VEGF transcripts at 3 and 24 hr. VEGF levels were significantly higher when h-SMC were cultured in medium containing ET-1 than when cultured in medium without ET-1. In conclusion, hypoxia and ET-1 constitute potent stimuli for VEGF production in h-SMC.
机译:血管内皮生长因子/血管通透性因子(VEGF / VPF)是血管内皮细胞分泌的促分裂原,在体内可促进血管通透性和新血管形成。我们研究了低氧张力在体外调节人主动脉血管平滑肌细胞(h-SMC)中VEGF表达的机制。此外,我们使用一种新开发的高度敏感的酶联免疫吸附测定法,在有或没有内皮素-1(ET-1)的情况下测量了培养基中的VEGF水平。缺氧导致在3和24小时大量诱导VEGF转录物。当在含有ET-1的培养基中培养h-SMC时,与在没有ET-1的培养基中培养相比,VEGF水平显着更高。总之,低氧和ET-1构成了h-SMC中VEGF产生的有效刺激。

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