Akt and Ca2+ signaling in endothelial cells
Akt and Ca2+ signaling in endothelial cells
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内皮细胞中的 Akt 和 Ca2 信号传导
DOI：
10.1023/b:mcbi.0000021369.17958.f4
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发表时间：
2004
影响因子：
4.3
通讯作者：
H. Hayashi
中科院分区：
文献类型：
--
作者：
Mariko Ozeki;Hiroshi Watanabe;Jinghui Luo;T. Nakano;K. Takeuchi;Y. Kureishi;Masa;T. Nakano;K. Ohashi;H. Hayashi
蛋白激酶Akt参与了内皮细胞的重要功能，如一氧化氮的产生和血管生成，这些活动涉及细胞内钙离子浓度的变化。然而，Akt的激活本身是否参与了这些细胞产生的钙信号的调节，目前还不清楚。本研究的目的是探讨Akt是否参与内皮细胞内钙信号的调节。用Fura-2对猪主动脉内皮细胞激动剂刺激的钙信号进行了比较，在对照组和Akt被不同的磷脂酰肌醇3-激酶(PI3)/Akt抑制剂或通过瞬时表达显性-阴性Akt(DnAkt)阻断Akt的情况下进行了比较。我们发现，缓激肽或thapsigargin刺激的细胞内钙库释放不受PI3激酶抑制剂LY294002和wortmannin的影响，也不受dnAkt表达的影响。LY294002呈剂量依赖性地抑制钙离子内流，这种作用在Wortmannin中看不到。DnAkt的表达对钙离子内流无影响。我们得出结论：Akt不参与激动剂刺激的内皮细胞内钙信号的调节。化合物LY294002通过一种不依赖于PI3激酶/Akt抑制的机制来抑制这些细胞内的钙离子内流。
The protein kinase Akt participates in such important functions of endothelial cells as nitric oxide production and angiogenesis, activities that involve changes in cytosolic Ca2+ concentration. However, it is not known if activation of Akt is itself involved in the regulation of Ca2+ signals produced in these cells. The objective of this study was to examine if Akt is involved in the regulation of Ca2+ signaling in endothelial cells. Agonist-stimulated Ca2+ signals, assessed using fura-2, were compared in porcine aortic endothelial cells under control conditions or conditions in which Akt was blocked either by different inhibitors of phosphatidylinositol 3-kinase (PI3 kinase)/Akt or by transient expression of a dominant-negative form of Akt (dnAkt). We found that the release of intracellular Ca2+ stores stimulated by bradykinin or thapsigargin is not affected by the PI3 kinase inhibitors LY294002 and wortmannin, or by expression of dnAkt. LY294002 dose-dependently inhibits store-operated Ca2+ entry, an effect not seen with wortmannin. Expression of dnAkt has no effect on store-operated Ca2+ entry. We conclude that Akt is not involved in the regulation of agonist-stimulated Ca2+ signals in endothelial cells. The compound LY294002 inhibits store-operated Ca2+ entry in these cells by a mechanism independent of PI3 kinase/Akt inhibition.
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DOI：
10.1042/bj2840521
发表时间：
1992-06
期刊：
The Biochemical journal
影响因子：
--
作者：
William P. Schilling;Olga A. Cabello;L. Rajan
通讯作者：
William P. Schilling;Olga A. Cabello;L. Rajan
影响因子：
56.9
作者：
L. Peso;M. González‐García;C. Page;R. Herrera;G. Núñez
通讯作者：
L. Peso;M. González‐García;C. Page;R. Herrera;G. Núñez
影响因子：
82.9
作者：
Kureishi, Y;Luo, ZY;Walsh, K
通讯作者：
Walsh, K
影响因子：
20.1
作者：
Morales-Ruiz, M;Fulton, D;Sessa, WC
通讯作者：
Sessa, WC
缓激肽诱导 Ca2 进入、释放和细胞内 Ca2 储备的再填充。
DOI：
--
发表时间：
1992
期刊：
The Journal of biological chemistry
影响因子：
--
作者：
Byron,KL;Babnigg,G;Villereal,ML
通讯作者：
Villereal,ML