Endothelium represents a defense barrier and responds and integrates neuro humoral stimulus which describes as a compensatory mechanism. Endothelium formed with endothelial cells (ECs) and their progenitors. Endothelial progenitor cells (EPCs) represent minor subpopulation of mononuclear cells in the blood. During acute hypoxia, larger amount of EPCs mobilize into the peripheral blood and they directly contribute revascularization process. One of the subtypes of EPC is termed endothelial colony forming cells (ECFCs) which they possess de novo vessel-forming ability. The present study aims to investigate the role of hypoxia in EPCs functional and vessel-forming ability. Furthermore, it was investigated whether fetal exposure to a diabetic intrauterine environment influence EPCs adaptation ability. Human umbilical cord blood (HUCB) derived ECFCs were selected in all experimental procedures obtained from normal and gestational diabetes mellitus (GDM) subjects via in vitro cell culture methods. Early passage (<5) HUCB ECFCs obtain from GDM (n; 5) and control (n; 5) subjects were cultured with plates pre-coated with collagen in vitro 72 h hypoxic as well as normoxic condition. Endothelial, angiogenic and hypoxia associated gene specific primers designed to perform Real-time PCR. Senescenes assay conducted onto HUCB ECFCs to investigate their functional clonogenic ability. To quantify their vessel forming ability matrigel assay was applied. These data demonstrates that moderate hypoxia results increased vessel-forming ability and VEGFA expression in HUCB ECFCs obtained from control subjects. However, GDM caused to impede compensatory defense reaction against hypoxia which observed in control subjects. Thus, it illuminates beneficial information related future therapeutic modalities.

中文翻译：

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适度的缺氧表现出内皮祖细胞形成能力的增强，但是妊娠期糖尿病会阻碍代偿性防御反应。

内皮代表防御屏障并响应和整合神经体液刺激，这被描述为一种补偿机制。内皮细胞由内皮细胞（EC）及其祖细胞形成。内皮祖细胞（EPC）代表血液中单核细胞的次要亚群。在急性缺氧期间，大量的EPC迁移到外周血中，它们直接有助于血运重建过程。EPC的一种亚型称为内皮集落形成细胞（ECFC），它们具有从头形成血管的能力。本研究旨在调查缺氧在EPC功能和血管形成能力中的作用。此外，研究了胎儿是否暴露于糖尿病子宫内环境是否会影响EPC的适应能力。通过体外细胞培养方法，从正常和妊娠糖尿病（GDM）受试者获得的所有实验程序中均选择了人脐带血（HUCB）衍生的ECFC。从GDM（n; 5）和对照（n; 5）受试者获得的早期传代（<5）HUCB ECFCs在体外缺氧和常氧条件下用预先涂有胶原蛋白的平板培养，培养时间为72 h。内皮，血管生成和缺氧相关的基因特异性引物，用于执行实时PCR。对HUCB ECFC进行了Senescenes分析，以研究其功能克隆能力。为了量化其血管形成能力，使用了基质胶测定法。这些数据表明，适度的缺氧导致从对照对象获得的HUCB ECFC中的血管形成能力和VEGFA表达增加。然而，GDM导致阻碍了在对照对象中观察到的针对缺氧的代偿性防御反应。因此，它阐明了与未来治疗方式有关的有益信息。