Vitamin D (1,25-(OH)(2)D(3)) Improves Endothelial Progenitor Cells Function via Enhanced NO Secretion in Systemic Lupus Erythematosus.

Vitamin D (1,25-(OH)(2)D(3)) Improves Endothelial Progenitor Cells Function via Enhanced NO Secretion in Systemic Lupus Erythematosus.
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维生素 D (1,25-(OH)(2)D-3) 通过增强系统性红斑狼疮中的 NO 分泌来改善内皮祖细胞功能

DOI:
10.1155/2020/6802562
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发表时间:
2020
影响因子:
2.1
通讯作者:
Jiang L
Jiang L
中科院分区:
医学4区
文献类型:
--
作者:
Huang Z;Liu L;Huang S;Li J;Feng S;Huang N;Ai Z;Long W;Jiang L

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系统性红斑狼疮(SLE)患者维生素D降低,循环内皮祖细胞(EPCs)功能受损。然而,维生素D对体外EPCs功能的影响及其机制有待进一步研究。因此,我们在体外研究维生素D是否能改善内皮祖细胞的功能。从SLE患者和对照组中分离受试者的外周血单个核细胞,培养成EPCs。用维生素D (1,25-(OH)2D3)处理EPCs后,我们在体外评估EPCs的数量、迁移和增殖活性以及一氧化氮(NO)的产生,并通过血流介导扩张(FMD)检测血管内皮功能。我们发现维生素D以剂量依赖的方式改善SLE患者EPCs的数量、迁移和增殖活性。此外,在体外实验中,维生素D可上调内皮祖细胞的NO生成。FMD与血浆NO水平有显著相关性。EPCs的数量、迁移和增殖与NO的产生也存在相关性。因此,本研究结果表明,维生素D通过NO分泌改善SLE患者EPCs的功能。
It has been proven that vitamin D was decreased and function of circulating endothelial progenitor cells (EPCs) was injured in systemic lupus erythematosus (SLE) patients. However, the effect of vitamin D on the function of EPCs in vitro and its mechanism need further study. Therefore, we investigated whether vitamin D improved the function of EPCs in vitro. The peripheral blood mononuclear cells of the participants were isolated from SLE patients and control subjects and cultured to EPCs. After the EPCs were treated with vitamin D (1,25-(OH)2D3), we evaluated the number, migratory and proliferative activities, and nitric oxide (NO) production of EPCs in vitro and detected vascular endothelial function by flow-mediated dilatation (FMD). We found that vitamin D in a dose-dependent manner improved number and migratory and proliferative activities of EPCs from SLE patients. Additionally, vitamin D upregulated NO production from EPCs in vitro. A significant correlation between the FMD and plasma NO level was found. There was also a correlation between number, migration, and proliferation of EPCs and NO production. Thus, the present findings indicated that vitamin D improved the function of EPCs from SLE patients via NO secretion.
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