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首页> 外文期刊>Journal of Cellular Physiology >Pro-inflammatory angiogenesis is mediated by p38 MAP kinase.
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Pro-inflammatory angiogenesis is mediated by p38 MAP kinase.

机译：促血管生成是由人们MAP激酶。

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摘要

Chronic inflammation is tightly linked to diseases associated with endothelial dysfunction including aberrant angiogenesis. To better understand the endothelial role in pro-inflammatory angiogenesis, we analyzed signaling pathways in continuously activated endothelial cells, which were either chronically exposed to soluble TNF or the reactive oxygen species (ROS) generating H2O2, or express active transmembrane TNF. Testing in an in vitro capillary sprout formation assay, continuous endothelial activation increased angiogenesis dependent on activation of p38 MAP kinase, NADPH oxidase, and matrix metalloproteinases (MMP). p38 MAP kinase- and MMP-9-dependent angiogenesis in our assay system may be part of a positive feed forward autocrine loop because continuously activated endothelial cells displayed up-regulated ROS production and subsequent endothelial TNF expression. The pro-angiogenic role of the p38 MAP kinase in continuously activated endothelial cells was in stark contrast to the anti-angiogenic activity of the p38 MAP kinase in unstimulated control endothelial cells. In vivo, using an experimental prostate tumor, pharmacological inhibition of p38 MAP kinase demonstrated a significant reduction in tumor growth and in vessel density, suggesting a pro-angiogenic role of the p38 MAP kinase in pathological angiogenesis in vivo. In conclusion, our results suggest that continuous activation of endothelial cells can cause a switch of the p38 MAP kinase from anti-angiogenic to pro-angiogenic activities in conditions which link oxidative stress and autocrine TNF production.
机译：慢性炎症疾病密切相关与内皮功能障碍包括有关异常的血管生成。内皮炎性作用血管生成,我们分析了信号通路不断激活内皮细胞,长期暴露于可溶性肿瘤坏死因子或吗活性氧(ROS)生成过氧化氢或跨膜TNF表达活跃。在体外测试毛细管发芽形成试验、连续内皮激活增加血管生成依赖激活p38 MAP激酶、NADPH氧化酶和矩阵金属蛋白酶(MMP)。MMP-9-dependent血管生成在我们的试验系统可能是一个积极的前馈自分泌的一部分吗不断循环,因为激活内皮细胞差异ROS生产和显示随后的内皮TNF的表达。pro-angiogenic p38 MAP激酶的作用不断激活内皮细胞形成鲜明对比的抗血管生成活性如果控制p38激酶地图内皮细胞。前列腺肿瘤,药理p38的抑制MAP激酶显著减少在肿瘤生长和血管密度,建议一个pro-angiogenic p38 MAP激酶的作用病理性血管生成体内。我们的研究结果表明,连续的激活内皮细胞可能导致p38的开关MAP激酶pro-angiogenic抗血管生成活动连接氧化条件压力和自分泌TNF生产。

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