Lu Wei, Su Le, Yu Zhezheng, Zhang Shangli, Miao Junying
Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Science, Shandong University, Jinan 250100, China.
Shandong Provincial Key Laboratory of Animal Cells and Developmental Biology, School of Life Science, Shandong University, Jinan 250100, China; The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education and Chinese Ministry of Health, Shandong University Qilu Hospital, Jinan 250012, China.
Stem Cells Int. 2016;2016:2539781. doi: 10.1155/2016/2539781. Epub 2016 Jan 6.
Bone marrow stromal cells (BMSCs) can differentiate into vascular endothelial cells (VECs). It is regarded as an important solution to cure many diseases, such as ischemic diseases and diabetes. However, the mechanisms underlying BMSC differentiation into VECs are not well understood. Recent reports showed that CD163 expression was associated with angiogenesis. In this study, overexpression of CD163 in BMSCs elevated the protein level of the endothelial-associated markers CD31, Flk-1, eNOS, and VE-cadherin, significantly increased the proportion of Alexa Fluor 488-acetylated-LDL-positive VECs, and promoted angiogenesis on Matrigel. Furthermore, we demonstrated that CD163 acted downstream homeobox containing 1 (Hmbox1) and upstream fibroblast growth factor 2 (FGF-2). These data suggested that CD163 was involved in Hmbox1/CD163/FGF-2 signal pathway in BMSC differentiation into vascular endothelial-like cells. We found a new signal pathway and a novel target for further investigating the gene control of BMSC differentiation into a VEC lineage.
骨髓基质细胞（BMSCs）可分化为血管内皮细胞（VECs）。这被视为治疗许多疾病的重要方法，如缺血性疾病和糖尿病。然而，BMSCs分化为VECs的潜在机制尚未完全明确。最近的报告显示，CD163的表达与血管生成有关。在本研究中，BMSCs中CD163的过表达提高了内皮相关标志物CD31、Flk-1、eNOS和VE-钙黏蛋白的蛋白水平，显著增加了Alexa Fluor 488-乙酰化低密度脂蛋白阳性VECs的比例，并促进了基质胶上的血管生成。此外，我们证明CD163作用于含同源框1（Hmbox1）的下游和成纤维细胞生长因子2（FGF-2）的上游。这些数据表明，CD163参与了BMSCs分化为血管内皮样细胞的Hmbox1/CD163/FGF-2信号通路。我们发现了一条新的信号通路和一个新的靶点，用于进一步研究BMSCs分化为VEC谱系的基因调控。
