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首页> 外文期刊>American Journal of Physiology >Effect of endothelial cell polarity on beta-amyloid-induced migration of monocytes across normal and AD endothelium.
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Effect of endothelial cell polarity on beta-amyloid-induced migration of monocytes across normal and AD endothelium.

机译：内皮细胞极性对β-淀粉样蛋白诱导的单核细胞跨正常和AD内皮迁移的影响。

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During normal aging and amyloid beta-peptide (Abeta) disorders such as Alzheimer's disease (AD), one finds increased deposition of Abeta and activated monocytes/microglial cells in the brain. Our previous studies show that Abeta interaction with a monolayer of normal human brain microvascular endothelial cells results in increased adherence and transmigration of monocytes. Relatively little is known of the role of Abeta accumulated in the AD brain in mediating trafficking of peripheral blood monocytes (PBM) across the blood-brain barrier (BBB) and concomitant accumulation of monocytes/microglia in the AD brain. In this study, we showed that interaction of Abeta(1--40) with apical surface of monolayer of brain endothelial cells (BEC), derived either from normal or AD individuals, resulted in increased transendothelial migration of monocytic cells (HL-60 and THP-1) and PBM. However, transmigration of monocytes across the BEC monolayer cultivated in a Transwell chamber was increased 2.5-fold when Abeta was added to the basolateral side of AD compared with normal individual BEC. The Abeta-induced transmigration of monocytes was inhibited in both normal and AD-BEC by antibodies to the putative Abeta receptor, receptor for advanced glycation end products (RAGE), and to the endothelial cell junction molecule, platelet-endothelial cell adhesion molecule-1 (PECAM-1). We conclude that interaction of Abeta with the basolateral surface of AD-BEC induces cellular signaling, promoting transmigration of monocytes from the apical to basolateral direction. We suggest that Abeta in the AD brain parenchyma or cerebrovasculature initiates cellular signaling that induces PBM to transmigrate across the BBB and accumulate in the brain.
机译：在正常衰老和淀粉样β肽（Abeta）疾病（例如阿尔茨海默氏病（AD））期间，人们发现Abeta和活化的单核细胞/小胶质细胞在大脑中的沉积增加。我们以前的研究表明，Abeta与正常人脑微血管内皮细胞单层的相互作用会导致单核细胞的粘附和转运增加。相对地，关于在AD脑中积累的Abeta在介导跨血脑屏障（BBB）的外周血单核细胞（PBM）的运输以及在AD脑中伴随的单核细胞/小胶质细胞的积累的作用了解甚少。在这项研究中，我们表明Abeta（1--40）与源自正常或AD个体的脑内皮细胞（BEC）单层顶表面的相互作用导致单核细胞（HL-60和THP-1）和PBM。然而，与正常个体BEC相比，当将Abeta添加到AD的基底外侧时，单细胞跨Transwell室中培养的BEC单层的迁移增加了2.5倍。在正常和AD-BEC中，Abeta诱导的单核细胞迁移均受到抗Abeta受体，晚期糖基化终产物（RAGE）受体和内皮细胞连接分子血小板-内皮细胞粘附分子-1抗体的抑制（PECAM-1）。我们得出结论，Abeta与AD-BEC的基底外侧表面的相互作用诱导细胞信号传导，促进单核细胞从顶端方向向基底外侧方向的迁移。我们建议AD脑实质或脑血管系统中的Abeta启动细胞信号传导，从而诱导PBM跨BBB迁移并积聚在大脑中。

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