Role of vitamin D in endothelial function and endothelial repair in clinically stable systemic lupus erythematosus.

John Reynolds, David Ray, M Yvonne Alexander, Ian Bruce

Research output: Contribution to journalArticlepeer-review


BACKGROUND: Patients with systemic lupus erythematosus (SLE) have endothelial dysfunction and increased risk of cardiovascular disease. Endothelium-dependent dilatation (ED) is abnormal in patients with SLE, and endothelial repair mechanisms are also impaired. Myeloid angiogenic cells (MACs) promote angiogenesis to restore damaged vessels. Vitamin D deficiency is associated with cardiovascular disease in the general population and is prevalent in SLE. We aimed to assess the effect of vitamin D on endothelial repair and function. METHODS: Vitamin D deficient (30 ng/mL) and healthy controls (>20 ng/mL) were also recruited. Endothelial function was determined by the ratio of ED to independent dilatation (EI). MACs from patients were cultured with and without 10 nM calcitriol, and function determined by migration and angiogenesis assays. Endothelial nitric oxide synthase (eNOS) expression was studied in human aortic endothelial cells treated with tumour necrosis factor α (TNFα) and MAC-conditioned media. FINDINGS: We studied 22 vitamin D deficient and 18 replete patients. Vitamin D deficient patients had an increased number of MACs compared with controls (p=0·04) but impaired migratory capacity (p=0·001) and reduced angiogenic capacity, although this was not statistically significant (p=0·13). Media from calcitriol-treated MACs significantly increased angiogenesis compared with untreated MACs (p=0·01). Calcitriol reduced IP-10 expression by MACs (p
Original languageEnglish
JournalLancet (London, England)
Volume385 Suppl 1
Publication statusPublished - 26 Feb 2015


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