Decreased endothelin receptor A autoantibody levels are associated with early ischaemic events in patients with giant-cell arteritis
| Autor: | Sebastian Klapa, Andreas Koch, Peter Lamprecht, Harald Heidecke, Susanne Schinke, Juliane Junker, Gabriela Riemekasten, Wataru Kähler, Antje Müller |
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| Rok vydání: | 2019 |
| Předmět: |
0301 basic medicine
Male medicine.medical_specialty Vascular smooth muscle Intimal hyperplasia Immunology Giant Cell Arteritis Inflammation General Biochemistry Genetics and Molecular Biology 03 medical and health sciences 0302 clinical medicine Rheumatology Ischemia Internal medicine medicine Immunology and Allergy Humans Arteritis Longitudinal Studies Aged Autoantibodies 030203 arthritis & rheumatology Aged 80 and over business.industry Autoantibody Middle Aged medicine.disease Receptor Endothelin A Endothelin 1 Giant cell arteritis 030104 developmental biology Endocrinology Cross-Sectional Studies cardiovascular system Female medicine.symptom Endothelin receptor business |
| Zdroj: | Annals of the rheumatic diseases. 78(10) |
| ISSN: | 1468-2060 |
| Popis: | 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 To address … |
| Databáze: | OpenAIRE |
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