Department of Pharmacology and Therapeutics, University of Florida, Gainesville, Florida, USA.
Microvasc Res. 2010 May;79(3):207-16. doi: 10.1016/j.mvr.2010.02.011. Epub 2010 Feb 25.
Bone-marrow-derived endothelial progenitor cells (EPCs) contribute to angiogenesis-mediated pathological neovascularization, and recent studies have begun to recognize the biological significance of this contribution. This review will discuss the ability of EPCs to contribute to neovascularization in both physiological and pathological conditions. Circulating EPCs were originally identified in 1997 by Asahara as CD34(+) VEGFR2(+) mononuclear cells. These cells differentiated into an endothelial phenotype, expressed endothelial markers, and incorporated into neovessels at sites of ischemia (Asahara et al., 1997). EPCs provide both instructive (release of pro-angiogenic cytokines) and structural (vessel incorporation and stabilization) functions that contribute to the initiation of neo-angiogenesis. EPC populations can be characterized based on surface markers of freshly isolated cells, or they can be described by their in vitro characteristics once placed in culture. However, a major stumbling block to progress in the field has been the lack of consensus among investigators as to the optimal characterization of EPCs. This review intends to address the role of both EPC classes and evaluate how they interact in the setting of pathological angiogenesis. Since the EPCs may be responsible for turning on the "angiogenic switch," strategies have been employed to keep this switch in the "off" position for diseases like cancer, retinopathy, and wet AMD. The expectation is that EPCs will evolve into clinically useful prognostic and predictive tools in cancer and in ocular diseases associated with pathological neovascularization and that targeting this cell type is a key to successful management of patients suffering from diseases associated with pathological neovascularization.
骨髓来源的内皮祖细胞 (EPCs) 有助于血管生成介导的病理性新生血管形成，最近的研究开始认识到这种贡献的生物学意义。本综述将讨论 EPC 在生理和病理条件下促进新生血管形成的能力。1997 年，Asahara 最初将循环 EPC 鉴定为 CD34(+) VEGFR2(+) 单核细胞。这些细胞分化为内皮表型，表达内皮标志物，并在缺血部位整合到新血管中 (Asahara 等人，1997 年)。EPC 提供指令性 (释放促血管生成细胞因子) 和结构性 (血管整合和稳定) 功能，有助于新血管生成的启动。EPC 群体可以根据新鲜分离细胞的表面标志物进行特征描述，也可以在放入培养后根据其体外特征进行描述。然而，该领域进展的主要障碍是研究人员对 EPC 最佳特征描述缺乏共识。本综述旨在探讨这两类 EPC 的作用，并评估它们在病理性血管生成中的相互作用。由于 EPC 可能负责开启“血管生成开关”，因此已经采用了各种策略来使该开关在癌症、视网膜病变和湿性 AMD 等疾病中保持关闭状态。期望 EPC 将演变为癌症和与病理性新生血管形成相关的眼部疾病中具有临床应用价值的预后和预测工具，并且靶向这种细胞类型是成功管理与病理性新生血管形成相关疾病患者的关键。
