...
首页> 外文期刊>Journal of Cellular Physiology >Hemin promotes proliferation and differentiation of endothelial progenitor cells via activation of AKT and ERK.
【24h】

Hemin promotes proliferation and differentiation of endothelial progenitor cells via activation of AKT and ERK.

机译:氯高铁血红素促进增殖和分化通过激活的内皮祖细胞AKT和ERK。

获取原文
获取原文并翻译 | 示例
           

摘要

Increased neovascularization is commonly observed in hemorrhagic plaques and associated with rupture of atherosclerotic lesions. This study aims to investigate whether hemin accumulated at the site of hematoma promotes neovascularization through affecting the growth and function of endothelial progenitor cells (EPCs) and the possible mechanism involved. Here we demonstrated that hemin promoted a significant increase in neovessel formation in matrigel plugs embedded in vivo and enhanced the proliferation and endothelial gene expression in EPCs in vitro. VEGF-induced migration response and the capability to incorporate into the vascular networks were markedly enhanced in hemin-treated EPCs. Hemin induced the phosphorylation of ERK and AKT but not p38 or JNK. The inhibition of AKT or ERK activation significantly attenuated the effect of hemin on cell proliferation. However, the enhanced migration response induced by hemin was significantly suppressed by the inhibition of AKT but not ERK. Hemin induced significant increase in reactive oxygen species (ROS) production and hemin-induced angiogenic response of EPCs was substantially reduced by treatment with N-acetylcysteine. Collectively, these data support that hemin-induced ROS mediates the activation of AKT and ERK signaling pathways, which in turn promotes the cell proliferation and function of EPCs. J. Cell. Physiol. 219: 617-625, 2009. (c) 2009 Wiley-Liss, Inc.
机译:增加新血管形成通常被观察到在出血性斑块和相关破裂动脉粥样硬化病变。旨在调查是否氯高铁血红素积累血肿的促进新血管形成通过影响的生长和功能内皮祖细胞(epc)和可能的机制。氯高铁血红素促进显著增加neovessel形成基底膜基质插头嵌入体内扩散和增强在内皮祖细胞体外内皮基因表达。VEGF-induced迁移反应,能力将进入血管网络在hemin-treated明显增强内皮祖细胞。和AKT但不是p38或物。或ERK激活明显减弱氯高铁血红素对细胞增殖的影响。增强的迁移氯高铁血红素引起的反应显著抑制抑制的一种蛋白激酶但不兵。增加活性氧(ROS)生产和hemin-induced血管生成反应大大降低了内皮祖细胞治疗有防治作用。支持hemin-induced ROS介导激活一种蛋白激酶ERK信号通路,进而促进细胞增殖和内皮祖细胞的功能。2009.

著录项

相似文献

  • 外文文献
  • 中文文献
获取原文

客服邮箱:kefu@zhangqiaokeyan.com

京公网安备:11010802029741号 ICP备案号:京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有
  • 客服微信

  • 服务号