中文摘要：

Angiogenesis 在愈合弯屈是关键的。mechano 生长因素(MGF24E ) 的 C 终端 24-a .a 肽的管理以前被表明了在与控制相比在有缺点的区域附近改革骨头导致更多的血容器。因此，这研究试图决定 MGF24E 是否支持骨头缺点通过增加 MGF24E 的 angiogenesis 愈合并且 MGF24E 是否在 vitro 在 angiogenesis 上有积极效果。angiogenesis 和内在的机制上的 MGF24E 的角色被调查。人的脉管的 endothelial EA.hy926 房间的房间增长，迁居，和 tubulogenesis 与 2% 浆液和 MGF24E 共同对待被决定与脉管的 endothelial 生长因素 165 的 100 ng/ml (VEGF165 ) 比较估计 angiogenesis 积极控制或车辆控制(缓冲磷酸盐盐) 。MGF24E 处理(10 ng/ml ) 显著地与车辆控制相比在 EA.hy926 房间上支持了 angiogenesis 的生物进程。脉管的 endothelial 生长因素和 angiopoietin 的抑制 -- 我由 2% 浆液饥饿的表情被 MGF24E 的 10 ng/ml 的增加在 2% 浆液媒介颠倒。这结果建议 MGF24E 在 angiogenesis 上有保护的效果。而且，分别地，而导致 MGF24 的 tubulogenesis 和 angiogenic 因素表示仅仅部分被禁止，英皇家空军之阶级最低之兵的抑制完全由于 PD98050 预告的处理废除了并且主要堵住了导致 MGF24E 的增长和移植。这些新调查结果建议 MGF24E 由提高包含 MAPK/ERK-signaling 小径的 angiogenic cytokines 的表示支持 angiogenesis。

英文摘要：

Angiogenesis is crucial in wound healing. The administra- tion of the C-terminal 24-a.a. peptide of mechano growth factor （MGF24E） has been previously demonstrated to induce more blood vessels in regenerating bone around defective areas compared with the control. Accordingly, this study aims to determine whether MGF24E promotes bone defect healing through MGF24E-increased angio- genesis and whether MGF24E has positive effects on angiogenesis in vitro. The roles of MGF24E on angiogen- esis and the underlying mechanisms were investigated. The cell proliferation, migration, and tubulogenesis of the human vascular endothelial EA.hy926 cells co-treated with 2% serum and MGF24E were determined to assess angiogenesis in comparison with 100 ng/ml of vascular endothelial growth factor 165 （VEGF16s）-positive control or vehicle control （phosphate-buffered saline）. MGF24E treatment （10 ng/ml） significantly promoted the biological processes of angiogenesis on EA.hy926 cells compared with the vehicle control. The suppression of vascular endothelial growth factor and angiopoietin-I expressions by 2% serum starvation was reversed by the addition of 10 ng/ml of MGF24E in 2% serum medium. This result suggests that MGF24E has a protective effect on angio- genesis. Moreover, the inhibition of ERK due to PD98050 pretreatment completely abolished and mostly blocked MGF24E-induced proliferation and migration, respective- ly, whereas the MGF24-induced tubulogenesis and the angiogenic factor expression were only partially inhibited. These new findings suggest that MGF24E promotes angiogenesis by enhancing the expression of angiogenic cytokines which involves the MAPK/ERK-signaling pathway.