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首页> 外文期刊>Molecular and Cellular Biochemistry: An International Journal for Chemical Biology >The role of SDF-1α/Rac pathway in the regulation of endothelial progenitor cell polarity; Homing and expression of Rac1, Rac2 during endothelial repair
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The role of SDF-1α/Rac pathway in the regulation of endothelial progenitor cell polarity; Homing and expression of Rac1, Rac2 during endothelial repair

机译:SDF-1α/ Rac通路在调节内皮祖细胞极性中的作用;内皮修复过程中Rac1,Rac2的归巢和表达

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The Stromal cell-derived factor-1 (SDF-1)/CXC chemokine receptor 4 (CXCR4) system is considered to be of great importance in diseases involving cardiogenesis and angiogenesis. The SDF-1α-RAC signaling pathway plays a pivotal role in a cell's polarity and serves to activate cell morphology variation and to control the direction of migration. We aimed to study whether the polarity of endothelial progenitor cells (EPCs) is changed by the induction of the SDF-1α-RAC signaling pathway, to investigate the mechanism of the effect of polarity on the homing action of EPCs, and to explore the gene and protein expression of Rac1/2 during endothelial repair. We measured the EPC characteristics of polarity induced by various final concentrations of SDF-1α; our observations included morphology variation, migration direction, and excursion. Of the dynamic variation and cytoskeleton rearrangement of EPCs induced by different final concentrations of SDF-1α, the most obvious variation was exhibited at the SDF-1α concentration of 200 ng/ml. Obvious polarity variations were also found in the EPCs and signal receptors induced by the SDF-1α concentration of 200 ng/ml. The Western blot analysis of Rac1 and Rac2 showed that the addition of AMD 3100 significantly inhibited the expression of Rac. The SDF-1α pathway potentially regulates the expression of Rac1/2. The actual excursion vector and the direction of the migration of EPCs induced by SDF-1α follows polarity, thus indicating the importance of further exploration regarding the homing induction of EPCs.
机译:基质细胞衍生因子1(SDF-1)/ CXC趋化因子受体4(CXCR4)系统被认为在涉及心源性和血管生成的疾病中非常重要。 SDF-1α-RAC信号通路在细胞极性中起关键作用,并用于激活细胞形态变化并控制迁移方向。我们旨在研究通过诱导SDF-1α-RAC信号通路是否改变内皮祖细胞(EPC)的极性,研究极性对EPC归巢作用的机制,并探索该基因修复过程中Rac1 / 2的表达和蛋白表达我们测量了各种最终浓度的SDF-1α引起的极性的EPC特性;我们的观察包括形态变化,迁移方向和偏移。在最终浓度不同的SDF-1α诱导的EPC的动态变化和细胞骨架重排中,最明显的变化出现在200 ng / ml的SDF-1α浓度下。在浓度为200 ng / ml的SDF-1α诱导的EPC和信号受体中也发现了明显的极性变化。 Rac1和Rac2的蛋白质印迹分析表明,添加AMD 3100可以显着抑制Rac的表达。 SDF-1α途径可能调节Rac1 / 2的表达。由SDF-1α诱导的EPC的实际偏移矢量和迁移方向遵循极性,因此表明了进一步探索有关EPC归巢诱导的重要性。

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