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Decreased endothelin receptor A autoantibody levels are associated with early ischaemic events in patients with giant-cell arteritis
  1. Sebastian Klapa1,2,
  2. Antje Müller1,
  3. Andreas Koch2,
  4. Harald Heidecke3,
  5. Wataru Kähler2,
  6. Juliane Junker3,
  7. Susanne Schinke1,
  8. Gabriela Riemekasten1,
  9. Peter Lamprecht1
  1. 1 Department of Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany
  2. 2 Institute of Experimental Medicine c/o German Naval Medical Institute, Christian-Albrechts-University Kiel, Kronshagen, Germany
  3. 3 CellTrend GmbH, Luckenwalde, Brandenburg, Germany
  1. Correspondence to Dr Sebastian Klapa, Rheumatology and Clinical Immunology, University of Lübeck, Lübeck, Germany; sebastian.klapa{at}uksh.de

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Endothelin 1 (ET-1) is a potent vasoactive peptide hormone produced by endothelial cells, macrophages and vascular smooth muscle cells (VSMCs). Elevated ET-1 plasma levels have been reported in patients with ischaemic complications in giant-cell arteritis (GCA), a systemic vasculitis predominantly affecting large vessels and their branches.1 In temporal artery biopsy specimens, increased expression of ET-1 and the G protein-coupled vasoconstrictive endothelin receptor A (ETAR) has been found.2 ETAR activation induces focal adhesion kinase-mediated morphological changes and increased motility of VSMC potentially contributing to intimal hyperplasia and vascular occlusion in GCA.3 VSMC migration can be blocked by specific ETAR antagonists.3 Notably, disease-specific anti-G protein-coupled receptor autoantibody (aab) signatures have been found in different autoimmune diseases.4 5 Anti-ETAR aabs are increased and associated with pulmonary arteriolar occlusion and hypertension in systemic sclerosis.5 6 Anti-ETAR aabss induce vascular adhesion molecules, interleukin (IL)-8 and chemokine ligand CCL-18 productions and exhibit chemotactic activity by mediating neutrophil and T cell migration.5 6

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