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首页> 外文期刊>Biochemistry and Cell Biology >Knockdown of Nrf2 inhibits angiogenesis by downregulating VEGF expression through PI3K/Akt signaling pathway in cerebral microvascular endothelial cells under hypoxic conditions
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Knockdown of Nrf2 inhibits angiogenesis by downregulating VEGF expression through PI3K/Akt signaling pathway in cerebral microvascular endothelial cells under hypoxic conditions

机译：NRF2的敲低通过在缺氧条件下通过脑微血管内皮细胞中的PI3K / AKT信号通路下调VEGF表达来抑制血管生成

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摘要

Ischemic stroke is a major cerebrovascular disease resulting from a transient or permanent local reduction of cerebral blood flow. Angiogenesis plays an important role in cerebral microvascular repair after ischemic stroke. This study aimed at investigating the effect of NF-E2-related factor 2 (Nrf2) on the angiogenesis of mouse cerebral microvascular endothelial bEnd.3 cells in a hypoxic environment. We found that Nrf2 expression was temporarily increased in hypoxia-induced bEnd.3 cells. Knockdown of Nrf2 inhibited the proliferation, migration, as well as tube formation in hypoxia-induced bEnd.3 cells. Meanwhile, vascular endothelial growth factor and PI3K/Akt signaling pathways were identified to be regulated by Nrf2 in hypoxia-induced bEnd.3 cells. It was found that silencing of Nrf2 downregulated the expression levels of NAD(P)H:quinine oxidoreductase-1, vascular endothelial growth factor, p-Akt, and heme oxygenise-1 in hypoxia-induced bEnd.3 cells. Data suggested that hypoxia induced the transient increase of Nrf2, which plays a key role in the angiogenesis of cerebral microan-giogenesis, and that Nrf2 regulates the proliferation, migration, as well as tube formation likely through PI3K/Akt signaling pathway in hypoxia-induced bEnd.3 cells. Our study provides proof of concept for the modulation of Nrf2, so as to tilt the balance toward angiogenesis, representing a therapeutic strategy for hypoxia or ischemia disorders such as stroke.
机译：缺血性中风是一种主要的脑血管疾病，由瞬态或永久性局部减少脑血流量导致。血管生成在缺血性卒中后在脑微血管修复中起着重要作用。本研究旨在研究NF-E2相关因子2（NRF2）对缺氧环境中小鼠脑微血管内皮弯曲薄细胞血管生成的影响。我们发现NRF2表达暂时增加了缺氧诱导的弯曲的弯曲的细胞。 NRF2的敲低抑制了缺氧诱导的弯曲弯曲的增殖，迁移以及管形成。同时，鉴定了血管内皮生长因子和PI3K / AKT信号传导途径被NRF2在缺氧诱导的弯曲的弯曲中调节。发现NRF2的沉默下调了NAD（P）H：奎宁氧化还原酶-1，血管内皮生长因子，P-AKT和血红素氧化-1的表达水平在缺氧诱导的弯曲中的弯曲中的弯曲蛋白。数据表明，缺氧诱导NRF2的瞬时增加，这在脑微型血管生成的血管生成中起着关键作用，并且NRF2调节了可能通过缺氧诱导的PI3K / AKT信号通路的增殖，迁移以及管形成弯曲3细胞。我们的研究提供了对NRF2调制的概念证明，从而倾斜血管生成的平衡，代表缺氧或缺血障碍等中风的治疗策略。

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