Effect of vitamin D on endothelial progenitor cells function.
Effect of vitamin D on endothelial progenitor cells function.
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DOI：
10.1371/journal.pone.0178057
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发表时间：
2017
期刊：
影响因子：
3.7
通讯作者：
Lev EI
中科院分区：
文献类型：
--
作者：
Hammer Y;Soudry A;Levi A;Talmor-Barkan Y;Leshem-Lev D;Singer J;Kornowski R;Lev EI
内皮祖细胞（EPCs）是骨髓来源的细胞，在血管损伤后的内皮化和血管修复过程中发挥重要作用。糖尿病患者内皮祖细胞受损与内皮功能障碍、冠状动脉疾病（CAD）和不良临床结局有关。最近的证据表明，维生素D的活性激素骨化三醇对内皮和心血管系统具有有利的影响。关于维生素D对EPCs功能的影响的数据有限。研究骨化三醇对健康受试者和糖尿病患者EPCs的体外作用。招募了51名2型糖尿病患者（60±11岁，40%女性，HbA 1C：9.1±0.8%）和23名健康志愿者。分离内皮祖细胞并在有和没有骨化三醇的情况下培养。培养1周后，评价细胞形成集落形成单位（CFU）的能力、它们的活力（通过MTT测定测量）、KLF-10水平和血管生成标志物。在糖尿病患者中，暴露于骨化三醇的EPC中的EPC CFU和细胞活力高于未暴露于骨化三醇的EPC [EPC CFU：1.25（IQR 1.0-2.0）vs. 0.5（IQR 0.5-1.9），p < 0.001; MTT：0.62（IQR 0.44-0.93）vs. 0.52（IQR 0.31-0.62），p = 0.001]。暴露于维生素D的EPCs中KLF-10水平往往较高，血管生成标志物无差异。在健康受试者中，补充骨化三醇也导致更高的细胞活力[MTT：0.23（IQR 0.11-0.46）vs. 0.19（0.09-0.39），p = 0.04]，但在CFU计数或血管生成标志物方面没有差异。在糖尿病患者中，体外补充维生素D可提高EPCs形成集落和生存能力。需要进一步研究维生素D发挥其作用的机制。
Endothelial progenitor cells (EPCs) are a population of bone marrow-derived cells, which have an important role in the process of endothelialization and vascular repair following injury. Impairment of EPCs, which occurs in patients with diabetes, was shown to be related to endothelial dysfunction, coronary artery disease (CAD) and adverse clinical outcomes. Recent evidence has shown that calcitriol, the active hormone of vitamin D, has a favorable impact on the endothelium and cardiovascular system. There is limited data on the effect of vitamin D on EPCs function. To examine the in vitro effects of Calcitriol on EPCs from healthy subjects and patients with diabetes. Fifty-one patients with type 2 diabetes (60±11 years, 40% women, HbA1C: 9.1±0.8%) and 23 healthy volunteers were recruited. EPCs were isolated and cultured with and without calcitriol. The capacity of the cells to form colony-forming units (CFUs), their viability (measured by MTT assay), KLF-10 levels and angiogenic markers were evaluated after 1 week of culture. In diabetic patients, EPC CFUs and cell viability were higher in EPCs exposed to calcitriol vs. EPCs not exposed to calcitriol [EPC CFUs: 1.25 (IQR 1.0–2.0) vs. 0.5 (IQR 0.5–1.9), p < 0.001; MTT:0.62 (IQR 0.44–0.93) vs. 0.52 (IQR 0.31–0.62), p = 0.001]. KLF-10 levels tended to be higher in EPCs exposed to vitamin D, with no differences in angiopoietic markers. In healthy subjects, calcitriol supplementation also resulted in higher cell viability [MTT: 0.23 (IQR 0.11–0.46) vs. 0.19 (0.09–0.39), p = 0.04], but without differences in CFU count or angiopoietic markers. In patients with diabetes mellitus, in vitro vitamin D supplementation improved EPCs capacity to form colonies and viability. Further studies regarding the mechanisms by which vitamin D exerts its effect are required.