Alkaline pH-induced extracellular regulated protein kinase activation in brain microvascular endothelial cells: differential effects of Tris and lowered CO2.

Gregory T Motz, Mario Zuccarello, Robert M Rapoport
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引用次数: 2

Abstract

As it was previously reported that Tris-elevated pH acutely activated extracellular regulated protein kinase (ERK) in rat aorta smooth muscle cells, this study tested whether this finding could be extended to endothelial cells and, moreover, the relevance of this finding in brain microvascular endothelial cells with respect to respiratory-induced hypocapnic alkalosis. Exposure of bovine brain microvascular endothelial cells to pH 7.90 due to Tris for 15 and 30 min activated ERK twofold. In contrast, pH elevated to 7.75 and 7.90 by lowered percent CO2 failed to activate ERK (15, 30, and 60 min). These results suggest that respiratory alkalosis due to hypocapnia does not activate ERK in brain microvascular endothelial cells. The ability of Tris to activate ERK suggests a novel pathway, possibly independent of pH elevation, whereby Tris activates ERK.

碱性ph诱导的脑微血管内皮细胞胞外调节蛋白激酶活化:Tris和降低CO2的差异效应。
正如之前报道的那样,tris升高的pH值急性激活了大鼠主动脉平滑肌细胞中的细胞外调节蛋白激酶(ERK),本研究测试了这一发现是否可以扩展到内皮细胞,此外,这一发现在脑微血管内皮细胞中与呼吸性低碳碱中毒的相关性。将牛脑微血管内皮细胞暴露于pH为7.90的Tris环境中15分钟和30分钟,ERK被激活两倍。相比之下,当pH值升高到7.75和7.90时,降低CO2的百分比,则无法激活ERK(15、30和60分钟)。这些结果表明,低碳酸血症引起的呼吸性碱中毒不会激活脑微血管内皮细胞中的ERK。Tris激活ERK的能力提示了一种可能独立于pH升高的新途径,即Tris激活ERK。
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