Vitamin D (1,25-(OH)2D3) Improves Endothelial Progenitor Cells Function via Enhanced NO Secretion in Systemic Lupus Erythematosus

Author:

Huang Zhenhua1ORCID,Liu Lixiang2,Huang Shufen1,Li Jianbo34,Feng Shaozhen34,Huang Naya34,Ai Zhen34,Long Weiqing5,Jiang Lanping34ORCID

Affiliation:

1. The Division of Emergency Medicine, The First Affiliated Hospital of Sun Yat-sen University, Guangzhou, China

2. Department of Gynecology, Seventh Affiliated Hospital of Sun Yat-sen University, Shenzhen, China

3. Department of Nephrology, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou 510080, China

4. Key Laboratory of Nephrology, National Health Commission and Guangdong Province, Guangzhou 510080, China

5. Department of Clinical Laboratory, The First Affiliated Hospital, Sun Yat-sen University, Guangzhou, China

Abstract

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.

Funder

National Natural Science Foundation of China

Publisher

Hindawi Limited

Subject

Cardiology and Cardiovascular Medicine

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