Translational Medical Sciences, School of Medicine, Biodiscovery Institute, University of Nottingham, Nottingham, NG7 2RD, UK.
Bucks Institute for Research on Aging, 8001 Redwood Blvd, Novato, CA, 94945, USA.
Stem Cell Rev Rep. 2024 Nov;20(8):2336-2344. doi: 10.1007/s12015-024-10777-5. Epub 2024 Aug 26.
Endothelial progenitor cells (EPCs) are stem cells that can repair injured blood vessels through neovascularisation. This is achieved through secretion of growth factors and endothelial maturation. EPC numbers and function have been studied to determine their diagnostic, prognostic and therapeutic potential in many ischaemic diseases such as stroke. However their activation homing and migration is not definitively understood in stroke patients. In this study, we profiled the non-stroke control group recruited into the Dunhill Medical Trust Endothelial Progenitor Cell Study. Demographic, clinical and plasma levels of angiogenic regulators of participants were analysed to determine if there was any correlation with EPC numbers, subtypes and function. Participants with diabetes had significantly supressed EPC numbers (CD45-CD34 + CD133 + KDR+) and CD34 + KDR + and KDR + EPC subtypes. Male participants had significantly lower EPC numbers compared to female participants and the proliferative capacity of endothelial colony forming cells significantly decreased with increasing participant age. Pro-angiogenic proteins such as granulocyte colony-stimulating factor and stromal cell-derived factor were positively correlated with both undifferentiated and endothelial-committed EPC subtype numbers (CD133+, KDR+, CD34 + CD133+, CD34 + KDR+), whereas anti-angiogenic proteins such as thrombospondin-1 showed a negative correlation with undifferentiated EPC subtypes (CD133+, CD34 + CD133+) but a positive correlation with endothelial-committed EPC subtype numbers (KDR+, CD34 + KDR+). These results show that EPC numbers and subtypes are affected by many factors and larger studies which can analyse and deconvolute the interactions between comorbidities, plasma biomarker levels and EPC are needed.
内皮祖细胞（EPC）是能够通过血管新生修复受损血管的干细胞。这是通过分泌生长因子和内皮成熟来实现的。已经研究了 EPC 的数量和功能，以确定它们在许多缺血性疾病（如中风）中的诊断、预后和治疗潜力。然而，中风患者中 EPC 的激活归巢和迁移尚未得到明确的理解。在这项研究中，我们对纳入邓希尔医学信托内皮祖细胞研究的非中风对照组进行了分析。分析了参与者的人口统计学、临床和血管生成调节剂的血浆水平，以确定它们与 EPC 数量、亚型和功能是否存在任何相关性。患有糖尿病的参与者的 EPC 数量（CD45-CD34+CD133+KDR+）和 CD34+KDR+和 KDR+EPC 亚型显著受到抑制。与女性参与者相比，男性参与者的 EPC 数量显著较低，内皮集落形成细胞的增殖能力随着参与者年龄的增加而显著降低。促血管生成蛋白，如粒细胞集落刺激因子和基质细胞衍生因子，与未分化和内皮定向 EPC 亚型数量（CD133+、KDR+、CD34+CD133+、CD34+KDR+）呈正相关，而抗血管生成蛋白，如血栓素-1，与未分化 EPC 亚型（CD133+、CD34+CD133+）呈负相关，但与内皮定向 EPC 亚型数量（KDR+、CD34+KDR+）呈正相关。这些结果表明，EPC 的数量和亚型受到许多因素的影响，需要进行更大的研究来分析和解卷积合并症、血浆生物标志物水平和 EPC 之间的相互作用。
