Hyperglycaemia exerts deleterious effects on late endothelial progenitor cell secretion actions
Hyperglycaemia exerts deleterious effects on late endothelial progenitor cell secretion actions
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DOI：
10.1177/1479164112444639
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发表时间：
2013-01
影响因子：
2.4
通讯作者：
Jie Zhang;Xiaoyun Zhang;Hong Li;Xiaodong Cui;Xiumei Guan;Kexin Tang;Chengwen Jin;Min Cheng
中科院分区：
文献类型：
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作者：
Jie Zhang;Xiaoyun Zhang;Hong Li;Xiaodong Cui;Xiumei Guan;Kexin Tang;Chengwen Jin;Min Cheng
内皮祖细胞（Endothelial progenitor cells，EPCs）通过分化为内皮细胞和分泌血管活性物质促进血管生成和维持血管稳态，在组织再生和血管修复中发挥重要作用。以前已经表明，高胆红素血症损害早期和晚期EPC功能，如分化、增殖和粘附。然而，其在EPCs，特别是晚期EPCs中调节血管活性物质产生的作用尚不明确。我们研究了高脂血症对晚期EPCs血管扩张因子、纤溶因子和血管生成生长因子的影响，以及对超氧化物歧化酶（SOD）活性的影响。采用酶联免疫吸附法（ELISA）检测不同浓度D-葡萄糖（5-40 mmol/L）孵育后EPCs中一氧化氮（NO）、组织型纤溶酶原激活物（t-PA）、纤溶酶原激活物抑制物-1（派-1）、前列腺素I2（PGI 2）、血管内皮生长因子（VEGF）的含量及超氧化物歧化酶（SOD）的活性。高糖应激条件下，晚期EPCs的NO、t-PA、派-1、PGI 2和VEGF水平均低于对照组（5 mmol/L葡萄糖）。此外，高糖还可降低晚期EPCs的SOD活性。这些结果表明，高血压引起的晚期EPC分泌功能的损害可能有助于糖尿病血管疾病的发展。
Endothelial progenitor cells (EPCs) play a fundamental role in tissue regeneration and vascular repair both by differentiating into endothelial cells and by secretion of vasoactive substances that promote angiogenesis and maintain vascular homeostasis. It has previously been shown that hyperglycaemia impairs early and late EPC functions, such as differentiation, proliferation and adhesion. However, its role in the regulation of the production of vasoactive substances in EPCs, especially in late EPCs, is less well defined. We investigated the effects of hyperglycaemia on the production of vasodilator, fibrinolytic and angiogenic growth factors, and also on the activity of superoxide dismutase (SOD) in late EPCs. For this purpose, late EPCs were incubated with different concentrations of D-glucose (5–40 mmol/L) for 24 hr. Levels of nitric oxide (NO), tissue plasminogen activator (t-PA), plasminogen activator inhibitor-1 (PAI-1), prostaglandin I2 (PGI2), vascular endothelial growth factor (VEGF) and the activity of SOD were measured by enzyme-linked immunosorbent assay (ELISA). Under high glucose stress conditions, late EPCs exhibited lower levels of NO, t-PA, PAI-1, PGI2 and VEGF compared to control medium (5 mmol/L glucose). Moreover, high glucose was also observed to decrease the activity of SOD in late EPCs. These results suggest that hyperglycaemia-induced impairment of late EPC secretion functions could contribute to the development of vascular disease in diabetes.