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首页> 外文期刊>The FEBS journal >Insulin-like growth factor-1 secreted by brain microvascular endothelial cells attenuates neuron injury upon ischemia.
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Insulin-like growth factor-1 secreted by brain microvascular endothelial cells attenuates neuron injury upon ischemia.

机译：脑微血管内皮细胞分泌的胰岛素样生长因子-1减轻缺血后神经元的损伤。

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Insulin-like growth factor (IGF)-1 is essential for the development of the nervous system, and is present in many cell types. Relatively little is known about IGF-1 expression in brain microvascular endothelial cells (BMECs). For in vivo studies, we examined the expression of IGF-1 and insulin-like growth factor-binding protein (IGFBP)-2 after focal cerebral ischemia for 12 h, 24 h, 3 days and 7 days, utilizing a permanent middle cerebral artery occlusion (MCAO) model in rats. For in vitro studies, we examined the levels of IGF-1 and IGFBP-2 in the culture medium or primary culture of BMECs injured by oxygen-glucose deprivation (OGD). Then, we elucidated the protective effects of IGF-1 on cortical neurons injured by OGD and the possible mechanism. In addition, we investigated the effect of BMEC-conditioned medium on IGF-1 receptor expression in neurons. The results showed that IGF-1 expression increased in serum and brain tissue, whereas IGFBP-2 expression decreased in brain tissue of MCAO-injured rats. In primary culture of BMECs, the expression levels of IGF-1 and IGFBP-2 were significantly higher under OGD conditions in culture. IGF-1 administration improved neuron viability upon normoxia or OGD, and upregulated p-Akt expression. This effect was reversed by LY294002, a specific inhibitor of the phosphoinositide 3-kinase-Akt signaling pathway. Furthermore, conditioned medium from OGD-treated BMECs substantially suppressed neuron viability and the expression of IGF-1 receptor simultaneously. These data demonstrate that therapeutic strategies that prioritize the early recovery of the IGF-1 system in BMECs might be promising in ischemic injury. 2013 FEBS.Registry Number/Name of Substance 0 (Culture Media, Conditioned). 0 (Insulin-Like Growth Factor Binding Protein 2). 67763-96-6 (Insulin-Like Growth Factor I). EC 2-7-10-1 (Receptor, IGF Type 1).
机译：胰岛素样生长因子（IGF）-1对于神经系统的发育至关重要，并且存在于许多细胞类型中。关于IGF-1在脑微血管内皮细胞（BMEC）中的表达了解相对较少。对于体内研究，我们利用一条永久性大脑中动脉检查了局灶性脑缺血12 h，24 h，3天和7天后IGF-1和胰岛素样生长因子结合蛋白（IGFBP）-2的表达大鼠闭塞（MCAO）模型。对于体外研究，我们检查了受氧-葡萄糖剥夺（OGD）伤害的BMEC的培养基或原代培养物中IGF-1和IGFBP-2的水平。然后，我们阐明了IGF-1对OGD损伤的皮质神经元的保护作用及其可能的机制。此外，我们调查了BMEC条件培养基对神经元中IGF-1受体表达的影响。结果表明，MCAO损伤的大鼠血清和脑组织中IGF-1表达增加，而脑组织中IGFBP-2表达减少。在BMEC的原代培养中，在培养的OGD条件下，IGF-1和IGFBP-2的表达水平显着升高。施用IGF-1可以改善常氧或OGD后神经元的活力，并上调p-Akt表达。磷酸肌醇3-激酶-Akt信号传导途径的特异性抑制剂LY294002逆转了这种作用。此外，来自OGD处理的BMEC的条件培养基可同时显着抑制神经元活力和IGF-1受体的表达。这些数据表明，优先考虑BMEC中IGF-1系统早期恢复的治疗策略在缺血性损伤中可能很有希望。 2013 FEBS。注册号/物质名称0（文化媒体，已处理）。 0（胰岛素样生长因子结合蛋白2）。 67763-96-6（胰岛素样生长因子I）。 EC 2-7-10-1（受体，IGF类型1）。

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