Tepper Oren M, Galiano Robert D, Capla Jennifer M, Kalka Christoph, Gagne Paul J, Jacobowitz Glen R, Levine Jamie P, Gurtner Geoffrey C
Laboratory of Microvascular Research and Vascular Tissue Engineering, Institute of Reconstructive Plastic Surgery, New York University Medical Center, New York, NY 10016, USA.
Circulation. 2002 Nov 26;106(22):2781-6. doi: 10.1161/01.cir.0000039526.42991.93.
The recent discovery of circulating endothelial progenitor cells (EPCs) has altered our understanding of new blood vessel growth such as occurs during collateral formation. Because diabetic complications occur in conditions in which EPC contributions have been demonstrated, EPC dysfunction may be important in their pathophysiology.
EPCs were isolated from human type II diabetics (n=20) and age-matched control subjects (n=20). Proliferation of diabetic EPCs relative to control subjects was decreased by 48% (P<0.01) and inversely correlated with patient levels of hemoglobin A1C (P<0.05). Diabetic EPCs had normal adhesion to fibronectin, collagen, and quiescent endothelial cells but a decreased adherence to human umbilical vein endothelial cells activated by tumor necrosis factor-alpha (TNF-alpha) (P<0.05). In a Matrigel assay, diabetic EPCs were 2.5 times less likely to participate in tubule formation compared with controls (P<0.05).
These findings suggest that type II diabetes may alter EPC biology in processes critical for new blood vessel growth and may identify a population at high risk for morbidity and mortality after vascular occlusive events.
循环内皮祖细胞（EPCs）的最新发现改变了我们对诸如侧支形成过程中发生的新血管生长的理解。由于糖尿病并发症发生在已证实有EPC参与的情况下，EPC功能障碍可能在其病理生理学中起重要作用。
从20例II型糖尿病患者和20例年龄匹配的对照受试者中分离出EPCs。与对照受试者相比，糖尿病EPCs的增殖降低了48%（P<0.01），且与患者糖化血红蛋白水平呈负相关（P<0.05）。糖尿病EPCs对纤连蛋白、胶原蛋白和静止内皮细胞具有正常的黏附能力，但对肿瘤坏死因子-α（TNF-α）激活的人脐静脉内皮细胞的黏附能力降低（P<0.05）。在基质胶试验中，与对照相比，糖尿病EPCs参与小管形成的可能性降低了2.5倍（P<0.05）。
这些发现表明，II型糖尿病可能在对新血管生长至关重要的过程中改变EPC生物学特性，并可能确定血管闭塞事件后发病和死亡风险较高的人群。
