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Oxidative stress tolerance of early stage diabetic endothelial progenitor cell

机译：早期糖尿病内皮祖细胞的氧化应激耐受性

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Introduction: One of the causes for poor vasculogenesis of diabetes mellitus (DM) is known to rise from the dysfunction of bone marrow-derived endothelial progenitor cells (BM EPCs). However, the origin of its cause is less understood. We aimed to investigate the effect of oxidative stress in early stage of diabetic BM-EPC and whether its vasculogenic dysfunction is caused by oxidative stress. Methods: Bone marrow c-Kit+Sca-1+Lin- (BM-KSL) cells were sorted from control and streptozotocin-induced diabetic C57BL6J mice by flow cytometry. BM-KSLs were then assessed for vasculogenic potential (colony forming assay; EPC-CFA), accumulation of intracellular ROS (CM-H2DCFDA), carbonylated protein (ELISA), anti-oxidative enzymes expression (RT-qPCR) and catalase activity (Amplex Red). Results: Compared to control, DM BM-KSL had significantly lower EPC-CFUs in both definitive EPC-CFU and total EPC-CFU (p < 0.05). Interestingly, the oxidative stress level of DM BM-KSL was comparable and was not significantly different to control followed by increased in anti-oxidative enzymes expression and catalase activity. Conclusions: Primitive BM-EPCs showed vasculogenic dysfunction in early diabetes. However the oxidative stress is not denoted as the major initiating factor of its cause. Our results suggest that primitive BM-KSL cell has the ability to compensate oxidative stress levels in early diabetes by increasing the expression of anti-oxidative enzymes.
机译：简介：众所周知，糖尿病（DM）血管生成不良的原因之一是源自骨髓源性内皮祖细胞（BM EPC）的功能障碍。但是，其起因尚不清楚。我们旨在研究氧化应激对糖尿病BM-EPC早期的影响，以及其血管生成功能障碍是否由氧化应激引起。方法：采用流式细胞术从对照组和链脲佐菌素诱导的糖尿病C57BL6J小鼠中分离骨髓c-Kit + Sca-1 + Lin-（BM-KSL）细胞。然后评估BM-KSL的血管生成潜力（集落形成测定; EPC-CFA），细胞内ROS积累（CM-H2DCFDA），羰基化蛋白（ELISA），抗氧化酶表达（RT-qPCR）和过氧化氢酶活性（Amplex红）。结果：与对照相比，DM BM-KSL在确定的EPC-CFU和总EPC-CFU中的EPC-CFU均显着降低（p <0.05）。有趣的是，DM BM-KSL的氧化应激水平相当，与对照无显着差异，随后抗氧化酶表达和过氧化氢酶活性增加。结论：原始BM-EPCs在早期糖尿病中显示出血管生成功能障碍。然而，氧化应激并未被认为是其原因的主要引发因素。我们的结果表明，原始BM-KSL细胞具有通过增加抗氧化酶的表达来补偿早期糖尿病中氧化应激水平的能力。

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