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Up-Regulation of ENO1 by HIF-1α in Retinal Pigment Epithelial Cells after Hypoxic Challenge Is Not Involved in the Regulation of VEGF Secretion

机译:缺氧攻击后视网膜色素上皮细胞中HIF-1α对ENO1的上调不参与VEGF分泌的调节

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摘要

PurposeAlpha-enolase (ENO1), a major glycolytic enzyme, is reported to be over-expressed in various cancer tissues. It has been demonstrated to be regulated by the Hypoxia-inducible factor 1-α (HIF-1α), a crucial transcriptional factor implicated in tumor progression and cancer angiogenesis. Choroidal neovascularization (CNV), which is a leading cause of severe vision loss caused by newly formed blood vessels in the choroid, is also engendered by hypoxic stress. In this report, we investigated the expression of ENO1 and the effects of its down-regulation upon cobalt (II) chloride-induced hypoxia in retinal pigment epithelial cells, identified as the primary source of ocular angiogenic factors.
机译:目的据报道,主要的糖酵解酶α-烯醇化酶(ENO1)在各种癌症组织中过表达。它已被证明由缺氧诱导因子1-α(HIF-1α)调节,缺氧诱导因子1-α(HIF-1α)是牵涉肿瘤进展和癌症血管生成的关键转录因子。脉络膜新血管形成(CNV)是由脉络膜中新形成的血管引起的严重视力丧失的主要原因,其原因还在于低氧应激。在这份报告中,我们调查了视网膜色素上皮细胞中ENO1的表达及其下调对氯化钴(II)诱导的缺氧的影响,视网膜色素上皮细胞被确定为眼血管生成因子的主要来源。

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