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首页> 外文期刊>Journal of Cellular Physiology >Angiotensin II-induced fluid phase endocytosis in human cerebromicrovascular endothelial cells is regulated by the inositol-phosphate signaling pathway.
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Angiotensin II-induced fluid phase endocytosis in human cerebromicrovascular endothelial cells is regulated by the inositol-phosphate signaling pathway.

机译：血管紧张素II-induced流体相内吞作用人类cerebromicrovascular内皮细胞肌醇磷酸盐信号调控途径。

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摘要

The involvement of the early signaling messengers, inositol tris-phosphate (IP3), intracellular calcium, [Ca2+]i, and protein kinase C (PKC), in angiotensin II (AII)-induced fluid phase endocytosis was investigated in human brain capillary and microvascular endothelial cells (HCEC). ALL (0.01-10 microM) stimulated the uptake of Lucifer yellow CH, an inert dye used as a marker for fluid phase endocytosis, in HCEC by 50-230%. AII also triggered a fast accumulation of IP3 and a rapid increase in [Ca2+]i in cells loaded with the Ca(2+)-responsive fluorescent dye fura-2. The prompt AII-induced [Ca2+]i spike was not affected by incubating HCEC in Ca(2+)-free medium containing 2 mM EGTA or by pretreating the cultures with the Ca2+ channel blockers, methoxyverapamil (D600; 50 microM), nickel (1 mM), or lanthanum (1 mM), suggesting that the activation of AII receptors on HCEC triggers the release of Ca2+ from intracellular stores. The AII-triggered increases in IP3, [Ca2+]i, and Lucifer yellow uptake were inhibited by the nonselective AII receptor antagonist, Sar1, Val5, Ala8-AII (SVA-AII), and by the phospholipase C (PLC) inhibitors, neomycin and U-73122. By contrast, the protein kinase C (PKC) inhibitors, staurosporine and calphostin C, failed to affect any of these AII-induced events. This study demonstrates that increased fluid phase endocytotosis induced by AII in human brain capillary endothelium, an event thought to be linked to the observed increases in blood-brain barrier permeability in acute hypertension, is likely dependent on PLC-mediated changes in [Ca2+]i and independent of PKC.
机译：早期的参与信号的信使,肌醇三磷酸酯(IP3),细胞内钙、[Ca2 +]我和蛋白激酶C (PKC)全身的血管紧张素ⅱ(暗)流体阶段内吞作用是研究人类的大脑毛细管和微血管内皮细胞(HCEC)。路西法黄色CH的吸收惰性染料用作流体相的标志内吞作用,HCEC50 - 230%。IP3和迅速增加[Ca2 +]我在细胞装满Ca(2 +)响应荧光染料fura-2。不受孵化HCEC在Ca (2 +)中包含2毫米EGTA或通过预处理文化与钙离子通道阻滞剂,methoxyverapamil (D600;毫米),或镧(1毫米),这表明激活HCEC受体触发暗生从细胞内释放Ca2 +的商店。AII-triggered IP3, [Ca2 +]我,路西法黄色的吸收受到抑制所有nonselective受体antagonist Sar1 Val5,Ala8-AII (SVA-AII)和磷脂酶C(PLC)抑制剂、新霉素和u - 73122。相反,蛋白激酶C (PKC)抑制剂,staurosporine和calphostin C,失败的影响这些AII-induced事件。表明,增加流体相endocytotosis引起人类大脑暗生毛细血管内皮细胞,被认为是一个事件观察增加血脑有关屏障通透性急性高血压可能依赖于PLC-mediated变化[Ca2 +]我对PKC和独立。

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