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首页> 外文期刊>Experimental & translational stroke medicine >The ATP-binding cassette transporters ABCB1 and ABCC1 are not regulated by hypoxia in immortalised human brain microvascular endothelial cells
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The ATP-binding cassette transporters ABCB1 and ABCC1 are not regulated by hypoxia in immortalised human brain microvascular endothelial cells

机译：ATP结合盒转运蛋白ABCB1和ABCC1在永生化的人脑微血管内皮细胞中不受缺氧的调节

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Background ATP-binding cassette transporters at the blood-brain barrier are actively regulated upon ischemic stroke in a way that impedes the access of pharmacological compounds to the brain tissue. The luminal endothelial transporter ABCB1 was recently shown to be increased, whereas the abluminal transporter ABCC1 was decreased on ischemic brain capillaries. In vitro studies using epithelial cells suggested that ABCB1 is regulated during hypoxia in a hypoxia-inducible factor (HIF)-1α-dependent way. Methods In order to investigate whether hypoxia might be responsible for the expression changes of ABCB1 and ABCC1 in the ischemic brain, the immortalised human brain microvascular endothelial cell line hCMEC/D3 was exposed to hypoxia (1%) or anoxia (0%). Cell lysates were analysed by Western blot to detect the protein expression of ABCB1, ABCC1, HIF-1α and HIF-2α. Results During hypoxia, an accumulation of HIF-1α and HIF-2α was noticed in hCMEC/D3 cells that followed different time kinetics. Both HIF-1α and HIF-2α abundance increased within 4 h of hypoxia. HIF-1α levels decreased to below detection levels within 16 h of hypoxia, whereas HIF-2α remained elevated even after 48 h. No changes of ABCB1 and ABCC1 expression were detected, neither on the mRNA nor protein level. Conclusion Our data suggests that other factors than hypoxia may be responsible for the expression changes of ATP-binding cassette transporters in the ischemic brain.
机译：血脑屏障处的背景ATP结合盒转运蛋白在缺血性卒中时受到积极调节，从而阻碍了药理化合物进入脑组织。最近显示，在缺血性脑毛细血管中，腔内内皮转运蛋白ABCB1增加，而腔内转运蛋白ABCC1减少。使用上皮细胞的体外研究表明，在缺氧期间以缺氧诱导因子（HIF）-1α依赖性方式调节ABCB1。方法为了研究缺氧可能是缺血脑中ABCB1和ABCC1表达变化的原因，将永生化的人脑微血管内皮细胞系hCMEC / D3暴露于缺氧（1％）或缺氧（0％）。通过蛋白质印迹分析细胞裂解物，以检测ABCB1，ABCC1，HIF-1α和HIF-2α的蛋白表达。结果缺氧期间，hCMEC / D3细胞中HIF-1α和HIF-2α的积累随时间的变化而变化。 HIF-1α和HIF-2α的丰度在缺氧4小时内增加。 HIF-1α水平在缺氧后16小时内降至检测水平以下，而HIF-2α即使在48小时后仍保持升高。没有检测到ABCB1和ABCC1表达的变化，无论是在mRNA还是蛋白水平上。结论我们的数据表明，缺氧以外的其他因素可能是缺血性脑中ATP结合盒转运蛋白表达变化的原因。

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