biostudies-literatureReynolds JAVersus ArthritisMedical Research CouncilNational Institute for Health Research (NIHR)Wellcome TrustBiotechnology and Biological Sciences Research Council22341https://www.ebi.ac.uk/biostudies/studies/S-EPMC4772382biostudies-literatureUnknown6Patients with systemic lupus erythematosus (SLE) have accelerated cardiovascular disease and dysfunctional endothelial repair mechanisms. Myeloid angiogenic cells (MACs), derived from circulating monocytes, augment vascular repair by paracrine secretion of pro-angiogenic factors. We observed that SLE MACs are dysfunctional and secrete pro-inflammatory cytokines. We also found that the vitamin D receptor was transiently expressed during MAC differentiation and that in vitro, calcitriol increased differentiation of monocytes into MACs in both SLE and in a model using the prototypic SLE cytokine, interferon-alpha. The active form of vitamin D (calcitriol) restored the SLE MAC phenotype towards that of healthy subjects with reduced IL-6 secretion, and normalised surface marker expression. CalcScientific reportsVitamin D improves endothelial dysfunction and restores myeloid angiogenic cell function via reduced CXCL-10 expression in systemic lupus erythematosus.PMC4772382MR/M008908/1NF-SI-0512-1010520380MR/L010240/1MANMKBRU-2012-1MR/L00254X/1G1000417/94909Ray DWBruce INReynolds JAWilliamson KAlexander MYHaque SfalseVitamin D improves endothelial dysfunction and restores myeloid angiogenic cell function via reduced CXCL-10 expression in systemic lupus erythematosus.Patients with systemic lupus erythematosus (SLE) have accelerated cardiovascular disease and dysfunctional endothelial repair mechanisms. Myeloid angiogenic cells (MACs), derived from circulating monocytes, augment vascular repair by paracrine secretion of pro-angiogenic factors. We observed that SLE MACs are dysfunctional and secrete pro-inflammatory cytokines. We also found that the vitamin D receptor was transiently expressed during MAC differentiation and that in vitro, calcitriol increased differentiation of monocytes into MACs in both SLE and in a model using the prototypic SLE cytokine, interferon-alpha. The active form of vitamin D (calcitriol) restored the SLE MAC phenotype towards that of healthy subjects with reduced IL-6 secretion, and normalised surface marker expression. Calc2016-01-01T00:00:00Z2016 Mar2025-05-29T21:40:21.163Z2025-05-29T21:40:21.163ZS-EPMC47723822693056710.1038/srep22341