Angiotensin II‐induced fluid phase endocytosis in human cerebromicrovascular endothelial cells is regulated by the inositol‐phosphate signaling pathway
Angiotensin II‐induced fluid phase endocytosis in human cerebromicrovascular endothelial cells is regulated by the inositol‐phosphate signaling pathway
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血管紧张素 II 诱导的人脑微血管内皮细胞液相内吞作用受肌醇磷酸信号通路的调节
DOI：
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发表时间：
1996
影响因子：
5.6
通讯作者：
J. Durkin
中科院分区：
文献类型：
--
作者：
D. Stanimirovic;P. Morley;R. Ball;E. Hamel;G. Mealing;J. Durkin
在人脑毛细血管和微血管内皮细胞（HCEC）中研究了早期信号信使三磷酸肌醇（IP 3）、细胞内钙离子[Ca 2 +]i和蛋白激酶C（PKC）参与血管紧张素II（AII）诱导的液相内吞作用。AII（0.01-10 μM）可刺激HCEC对荧光黄CH（一种用作液相内吞标记物的惰性染料）的摄取，使其增加50- 230%。AII还引发了负载Ca 2+响应性荧光染料fura-2的细胞中IP 3的快速积累和[Ca 2 +]i的快速增加。在含2 mM EGTA的无钙培养基中孵育HCEC或用钙通道阻断剂甲氧基维拉帕米（D 600; 50 μM）、镍（1 mM）或镧（1 mM）预处理培养物均不影响AII诱导的[Ca 2 +]i峰值，表明HCEC上AII受体的激活触发了细胞内钙库的Ca 2+释放。非选择性AII受体拮抗剂Sar 1、Val 5、Ala 8-AII（SVA-AII）和磷脂酶C（PLC）抑制剂新霉素和U-73122可抑制AII触发的IP 3、[Ca 2 +]i和荧光黄摄取增加。相比之下，蛋白激酶C（PKC）抑制剂staurosporine和calphostin C未能影响任何这些AII诱导的事件。本研究表明，AII诱导的人脑毛细血管内皮细胞液相内吞作用增加（被认为与急性高血压中观察到的血脑屏障通透性增加相关）可能依赖于PLC介导的[Ca 2 +]i变化，而不依赖于PKC。© 1996 Wiley利斯公司
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). AII (0.01–10 μM) 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 Ca2+‐responsive fluorescent dye fura‐2. The prompt AII‐induced [Ca2+]i spike was not affected by incubating HCEC in Ca2+‐free medium containing 2 mM EGTA or by pretreating the cultures with the Ca2+ channel blockers, methoxyverapamil (D600; 50 μM), 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. © 1996 Wiley‐Liss, Inc.
血管紧张素肽刺激内皮细胞前列腺素的产生。
DOI：
10.1161/01.hyp.19.2_suppl.ii49
发表时间：
1992
期刊：
Hypertension (Dallas, Tex. : 1979)
影响因子：
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作者：
Jaiswal,N;Diz,DI;Chappell,MC;Khosla,MC;Ferrario,CM
通讯作者：
Ferrario,CM
影响因子：
8.3
作者：
HIMMEL, HM;WHORTON, AR;STRAUSS, HC
通讯作者：
STRAUSS, HC