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首页> 外文期刊>Journal of Cellular Physiology >Apoptotic endothelial cells demonstrate increased adhesiveness for human mesenchymal stem cells.
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Apoptotic endothelial cells demonstrate increased adhesiveness for human mesenchymal stem cells.

机译:凋亡内皮细胞证明增加人类间充质干细胞的粘合度。

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摘要

Mesenchymal stem cells (MSCs) participate in the wound healing process in mammalians. Adhesion of MSCs to endothelium is a key step in the homing of MSCs circulating in the bloodstream to the sites of injury and inflammation. Because endothelial cells (ECs) may become apoptotic under certain pro-inflammatory conditions, we investigated the effects of pro-inflammatory, TNF-alpha and IL-1 beta, and pro-apoptotic agents, actinomycin D, cycloheximide, okadaic acid, wortmannin, and staurosporine, on human MSCs (hMSCs) adhesion to ECs. Treatment of ECs with pro-apoptotic agents markedly increased adhesion of hMSCs to ECs. This adhesion correlated with reduction of mitochondrial membrane potential, inhibition of NADH dehydrogenases, and release of von Willebrand factor (vWF) by ECs. Treatment of ECs with exogenous vWF also stimulated hMSC adhesion. These data provide evidence that apoptosis of ECs may regulate homing of hMSCs to the sites of tissue injury. These results are consistent with the hypothesis thatactivation of apoptotic signaling pathways in ECs releases vWF which regulates hMSC adhesion to ECs.
机译:间充质干细胞(msc)参与在哺乳动物的伤口愈合过程。msc归航的内皮是关键的一步msc在血液中循环的网站的损伤和炎症。内皮细胞(ECs)可能成为凋亡在某些炎性条件,我们研究促炎症的影响,tnf和il - 1β,pro-apoptotic代理、放线菌素D环己酰亚胺,冈田酸,渥曼青霉素,staurosporine人类msc (hMSCs)粘附ECs。与代理pro-apoptotic明显增加附着力hMSCs ECs。与减少线粒体膜电位,NADH的抑制血管性血友病的脱氢酶和发布ECs因子(vWF)。外生vWF也刺激hMSC附着力。这些数据提供的证据表明,细胞凋亡的ECs可以调节归航hMSCs的网站吗组织损伤。假设thatactivation凋亡信号通路在ECs释放vWF调节hMSC粘附ECs。

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