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首页> 外文期刊>Journal of Cellular Physiology >Protein kinase C beta 1 overexpression augments phorbol ester-induced increase in endothelial permeability.
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Protein kinase C beta 1 overexpression augments phorbol ester-induced increase in endothelial permeability.

机译:蛋白激酶Cβ1超表达增强佛波醇ester-induced增加内皮渗透率。

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摘要

We studied the postulated involvement of the protein kinase C beta 1 (PKC beta 1) isoform in the regulation of endothelial permeability using human dermal microvascular endothelial cell line (HMEC-1). We overexpressed the recombinant PKC beta 1 gene via retroviral-mediated transduction in these cells. PKC beta 1 gene transfer was stable, and PKC beta 1 protein production was persistent for at least 1 month posttransduction. Addition of 2 x 10(-9) M and 2 x 10(-8) M phorbol 12-myristate 13-acetate (PMA) to the control (nontransduced) HMEC-1 cells increased the transendothelial 125I-albumin clearance rate (an index of endothelial permeability) from 2.5 +/- 0.2 x 10(-2) microliters/min to 5.4 +/- 1.2 x 10(-2) microliters/min and 16.8 +/- 3.1 x 10(-2) microliters/min, respectively. However, addition of 2 x 10(-9) M PMA to PKC beta 1-overexpressing HMEC-1 cells produced a maximal increase in the transendothelial 125I-albumin clearance rate of 15.9 +/- 2.0 x 10(-2) microliters/min. Challenge of these cells with 2 x 10(-8) M PMA did not further augment the increase in permeability. Activation with PMA was associated with the translocation of the PKC beta 1 from the cytosol to the membrane. These data show that PKC beta 1 overexpression augments the increase in endothelial permeability in response to PKC activation, suggesting an important function for the PKC beta 1 isoform in the regulation of endothelial barrier.
机译:我们研究了假定的参与1β蛋白激酶C (PKCβ1)同种型血管内皮通透性的规定使用人类皮肤微血管内皮细胞(HMEC-1)。β1通过retroviral-mediated基因转导在这些细胞。稳定,PKC beta 1蛋白的生产持续至少1个月posttransduction。添加2 x 10 M和2 x(9) 10(8)米佛波醇12-myristate 13-acetate (PMA)控制(nontransduced) HMEC-1细胞增加了125年transendothelial i-albumin清除率(一个指数从2.5 + / -内皮通透性)0.2 x 10(2)每毫升/分钟5.4 + / - 1.2 x10(2)每毫升/分钟和16.8 + / - 3.1 x 10 (2)分别每毫升/分钟。2 x 10 (9) M PMA PKCβ1-overexpressingHMEC-1细胞产生极大增加125年transendothelial i-albumin清除率15.9 + / - 2.0 x 10(2)每毫升/分钟。这些细胞的2 x 10(8)米PMA没有进一步增强渗透性的增加。激活和PMA是相关的易位的PKC beta 1胞质膜。超表达增强的增加内皮渗透性对PKC的回应激活,这表明一个重要的函数在PKC beta 1对碘氧基苯甲醚的规定内皮屏障。

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