Boyd N L, Dhara S K, Rekaya R, Godbey E A, Hasneen K, Rao R R, West F D, Gerwe B A, Stice S L
University of Georgia, Regenerative Bioscience Center, Athens, GA 30602, USA.
Exp Biol Med (Maywood). 2007 Jun;232(6):833-43.
The vasculature develops primarily through two processes, vasculogenesis and angiogenesis. Although much work has been published on angiogenesis, less is known of the mechanisms regulating the de novo formation of the vasculature commonly called vasculogenesis. Human embryonic stem cells (hESC) have the capability to produce all of the cells of the body and have been used as in vitro models to study the molecular signals controlling differentiation and vessel assembly. One such regulatory molecule is bone morphogenetic protein-4 (BMP4), which is required for mesoderm formation and vascular/hematopoietic specification in several species. However, hESC grown in feeder-free conditions and treated with BMP4 differentiate into a cellular phenotype highly expressing a trophoblast gene profile. Therefore, it is unclear what role, if any, BMP4 plays in regulating vascular development in hESC. Here we show in two National Institutes of Health-registered hESC lines (BG02 and WA09) cultured on a 3D substrate of Matrigel in endothelial cell growth medium-2 that the addition of BMP4 (100 ng/ml) for 3 days significantly increases the formation and outgrowth of a network of cells reminiscent of capillary-like structures formed by mature endothelial cells (P<0.05). Analysis of the expression of 45 genes by quantitative real time-polymerase chain reaction on a low-density array of the entire culture indicates a rapid and significant downregulation of pluripotent and most ectodermal markers with a general upregulation of endoderm, mesoderm, and endothelial markers. Of the genes assayed, BMPR2 and RUNX1 were differentially affected by exposure to BMP4 in both cell lines. Immunocytochemistry indicates the morphological structures formed were negative for the mature endothelial markers CD31 and CD146 as well as the neural marker SOX2, yet positive for the early vascular markers of endothelium (KDR, NESTIN) and smooth muscle cells (alpha-smooth muscle actin [alpha SMA]). Together, these data suggest BMP4 can enhance the formation and outgrowth of an immature vascular system.
脉管系统主要通过血管生成和血管新生这两个过程发育而成。尽管关于血管新生已发表了大量研究,但对于调控通常被称为血管生成的血管系统从头形成的机制,人们了解得较少。人类胚胎干细胞(hESC)有能力生成身体的所有细胞,并已被用作体外模型来研究控制分化和血管组装的分子信号。一种这样的调节分子是骨形态发生蛋白-4(BMP4),它在几个物种中是中胚层形成以及血管/造血细胞特化所必需的。然而,在无饲养层条件下培养并用BMP4处理的hESC会分化为高度表达滋养层基因谱的细胞表型。因此,尚不清楚BMP4在调控hESC的血管发育中是否发挥作用,若有作用,其作用是什么。在此我们表明,在两种美国国立卫生研究院注册的hESC系(BG02和WA09)中,于内皮细胞生长培养基-2中的基质胶三维基质上培养时,添加BMP4(100 ng/ml)3天可显著增加类似于成熟内皮细胞形成的毛细血管样结构的细胞网络的形成和生长(P<0.05)。通过对整个培养物的低密度阵列进行定量实时聚合酶链反应分析45个基因的表达表明,多能性和大多数外胚层标记物迅速且显著下调,而内胚层、中胚层和内皮标记物普遍上调。在所检测的基因中,BMPR2和RUNX1在两种细胞系中受BMP4暴露的影响存在差异。免疫细胞化学表明,所形成的形态结构对成熟内皮标记物CD31和CD146以及神经标记物SOX2呈阴性,但对内皮早期血管标记物(KDR、巢蛋白)和平滑肌细胞(α-平滑肌肌动蛋白[α-SMA])呈阳性。这些数据共同表明,BMP4可增强未成熟血管系统的形成和生长。