中文摘要：

骨头导出髓的间充质的干细胞(BMSC ) 是有增长和区别的能力进间充质的系房间的 multipotent 祖先的一张人口。规章的肽 apelin 是为 G 联合蛋白质的受体 APJ 的内长的 ligand。Apelin，能提高 BMSC 增长，在许多房间类型上有 mitogenic 效果。我们假设了增加的 apelin/APJ 可能涉及导致组织缺氧的 BMSC 增长的出现和发展。从到 10-week-old C57BL/6J 老鼠的 8- 的骨头髓的 BMSC 在 normoxia (21% 氧) 或组织缺氧(1% 氧) 下面是有教养的状况。房间增长被 3-(4,5-dimethylthiazol-2-yl ) 决定 -2,5-diphenyltetrazolium 溴化物试金和 5-bromo-2-deoxyuridine 试金。组织缺氧可诱导的因素(HIF ) 的表情 -1, apelin， APJ， Beclin-1，和 LC3II/LC3I 被西方的污点分析检测。结果建议组织缺氧以一种时间依赖者方式提高了 BMSC 的增长。HIF-1， apelin， APJ， Beclin-1，和 LC3II/LC3I 的表情在组织缺氧导致的 BMSC 被增加。禁止了 apelin， APJ， Beclin-1，和 LC3II/LC3I 的导致组织缺氧的表情的小介入 RNA (siRNA )-HIF-1 阻止了导致组织缺氧的 BMSC 增长。禁止了 Beclin-1 和 LC3II/LC3I 的导致组织缺氧的表情的 siRNA-APJ 颠倒了导致组织缺氧的 BMSC 增长。siRNA-Beclin-1 也废除了导致组织缺氧的房间增长。这些数据建议表明小径的 apelin/APJ/autophagy 可能涉及导致组织缺氧的 BMSC 增长。

英文摘要：

Bone marrow-derived mesenchymal stem cells （BMSCs） are a population of multipotent progenitors that have the capacity of proliferation and differentiation into mesenchymal lineage cells. The regulatory peptide apelin is the endogenous ligand for the G protein-coupled receptor APJ. Apelin, which can enhance BMSC proliferation, has mitogenic effects on a wide variety of cell types. We hypothesized that the increased apelin/APJ might be involved in the occurrence and development of hypoxia-induced BMSC proliferation. BMSCs from the bone marrow of 8- to 10-week-old C57BL/6J mice were cultured under either normoxia （21% oxygen） or hypoxia （1% oxygen） condition. Cell pro- liferation was determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide assay and 5-bromo-2＇-deoxyuridine assay. Expressions of hypoxia-inducible factor （HIF）-1α, apelin, APJ, Beclin-1, and LC311/LC31 were detected by western blot analysis. Results suggested that hypoxia enhanced the proliferation of BMSC in a time-dependent manner. The expressions of HIF-1α, apelin, APJ, Beclin-1, and LC311/LC31 were increased in BMSCs induced by hypoxia. Small interfering RNA （siRNA）-HIF-lc（ that inhibited the hypoxia-induced expressions of apelin, APJ, Beclin-1, and LC311/ LC31 prevented hypoxia-induced BMSC proliferation, siRNA-APJ that inhibited the hypoxia-induced expressions of Beclin-1 and LC311/LC31 reversed hypoxia-induced BMSC proliferation, siRNA-Beclin- 1 also abolished hypoxia-induced cell proliferation. These data suggested that the apelin/APJ/autophagy signaling pathway might be involved in hypoxia-induced BMSC proliferation.