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Haematopoietic and endothelial progenitor cells are deficient in quiescent Systemic Lupus Erythematosus
  1. Peter E Westerweel (p.westerweel{at}umcutrecht.nl)
  1. UMC Utrecht, Netherlands
    1. Remco KMAC Luijten (r.luijten{at}umcutrecht.nl)
    1. UMC Utrecht, Netherlands
      1. Imo E Hoefer (i.hoefer{at}umcutrecht.nl)
      1. UMC Utrecht, Netherlands
        1. Hein A Koomans (h.a.koomans{at}azu.nl)
        1. UMC Utrecht, Netherlands
          1. Ronald HWM Derksen (r.h.w.m.derksen{at}azu.nl)
          1. UMC Utrecht, Netherlands
            1. Marianne C Verhaar (m.c.verhaar{at}umcutrecht.nl)
            1. UMC Utrecht, Netherlands

              Abstract

              Objectives:SLE is associated with a high prevalence of cardiovascular disease (CVD). Circulating Endothelial Progenitor Cells (EPC) contribute to vascular regeneration and repair, thereby protecting against atherosclerotic disease. EPC are derived from CD34+ Haematopoietic Stem Cells (HSC), which have an increased propensity for apoptosis in the bone marrow of SLE patients. We aimed to determine whether circulating HSC and EPC are reduced in SLE, contributing to an increased cardiovascular risk.

              Methods:Progenitor cells were sampled from 15 female SLE patients in prolonged clinical remission from their disease and 15 matching healthy controls. HSC and CD34+KDR+ EPC were quantified by flow cytometry. Annexin V staining was used to identify apoptotic cells.

              Results:SLE patients had reduced levels of circulating CD34+ HSC and CD34+KDR+ EPC, associated with increased HSC apoptosis. Compared to controls, the fraction of HSC that could be identified as EPC was higher in SLE patients, consistent with a primary defect of HSC. EPC outgrowth from mononuclear cells, which depends mainly on CD34-negative cells, was unaffected.

              Conclusions:SLE patients have lower levels of circulating HSC and EPC, even during clinical remission. Our data suggest that increased HSC apoptosis is the underlying cause for this depletion. These observations indicate that progenitor cell mediated endogenous vascular repair is impaired in SLE, which may contribute to the accelerated development of atherosclerosis.

              • Systemic Lupus Erythomatosus
              • atherosclerosis
              • endothelial progenitor cells
              • endothelium
              • haematopoietic stem cells

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