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首页> 外文期刊>Diabetes care >Diabetes impairs stem cell and proangiogenic cell mobilization in humans
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Diabetes impairs stem cell and proangiogenic cell mobilization in humans

机译：糖尿病损害人类干细胞和促血管生成细胞的动员

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OBJECTIVE-Diabetes mellitus (DM) increases cardiovascular risk, at least in part, through shortage of vascular regenerative cells derived from the bone marrow (BM). In experimental models, DM causes morphological and functional BM alterations, but information on BM function in human DMismissing. Herein, we sought to assaymobilization of stemand proangiogenic cells in subjects with and without DM. RESEARCH DESIGN AND METHODS-In a prospective trial (NCT01102699), we tested BM responsiveness to 5 ??g/kg human recombinant granulocyte colony-stimulating factor (hrG-CSF) in 24 individuals with DM (10 type 1 and 14 type 2) and 14 individuals without DM. Before and 24 h after hrG-CSF, we quantified circulating stem/progenitor cells and total and differential white blood cell counts. We also evaluated in vivo the proangiogenic capacity of peripheral blood mononuclear cells using the Matrigel plug assay. RESULTS-In response to hrG-CSF, levels of CD34+ cells and other progenitor cell phenotypes increased in subjects without DM. Patients with DM had significantly impaired mobilization of CD34+, CD133+, and CD34 +CD133+ hematopoietic stem cells and CD133 +KDR+ endothelial progenitors, independently of potential confounders. The in vivo angiogenic capacity of peripheral blood mononuclear cells significantly increased after hrG-CSF in control subjects without DM, but not in patients with DM. DM was also associated with the inability to upregulate CD26/DPP-4 on CD34+ cells, which is required for the mobilizing effect of granulocyte colony-stimulating factor. CONCLUSIONS-Stem and proangiogenic cell mobilization in response to hrG-CSF is impaired in DM, possibly because of maladaptive CD26/DPP-4 regulation. These alterations may hamper tissue repair and favor the development of cardiovascular complications. ? 2013 by the American Diabetes Association.
机译：目标糖尿病（DM）至少部分地由于缺乏源自骨髓（BM）的血管再生细胞而增加了心血管风险。在实验模型中，DM会引起BM形态和功能的改变，但有关DM在人类DM生理中的作用的信息。本文中，我们试图在患有和不患有DM的受试者中测定干细胞和促血管生成细胞的动员。研究设计和方法-在一项前瞻性试验（NCT01102699）中，我们在24名患有DM（10型1和14型2）的个体中测试了BM对5μg/ kg人重组粒细胞集落刺激因子（hrG-CSF）的反应性。和14个人没有DM。在hrG-CSF之前和之后24小时，我们对循环的干/祖细胞以及总白细胞和差异白细胞计数进行了定量。我们还使用Matrigel塞测定法评估了外周血单个核细胞的促血管生成能力。结果-对hrG-CSF的反应，无DM的受试者中CD34 +细胞和其他祖细胞表型的水平增加。 DM患者的CD34 +，CD133 +和CD34 + CD133 +造血干细胞以及CD133 + KDR +内皮祖细胞的动员能力显着受损，而与潜在的混杂因素无关。 hrG-CSF后，外周血单核细胞的体内血管生成能力在无DM的对照组中显着增加，而在DM患者中则没有。 DM还与无法上调CD34 +细胞上的CD26 / DPP-4有关，这是粒细胞集落刺激因子的动员作用所必需的。结论DM中hrG-CSF的干细胞和促血管生成细胞动员受损，可能是由于CD26 / DPP-4适应不良。这些改变可能会阻碍组织修复并有利于心血管并发症的发展。 ？ 2013年由美国糖尿病协会颁发。

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