26rhk046 10.3205/26rhk046 urn:nbn:de:0183-26rhk0460 Meeting Abstract Regulation of endothelial vascular adhesion protein-1 in giant cell arteritis Gheitasi Gheitasi Reza R
Universität Bonn, Uniklinikum Bonn, Medizinische Klinik und Poliklinik III Innere Medizin mit den Schwerpunkten Onkologie, Hämatologie und Rheumatologie, Bonn, Deutschland
author Petzinna Petzinna Simon M. SM
Universität Bonn, Uniklinikum Bonn, Medizinische Klinik und Poliklinik III Innere Medizin mit den Schwerpunkten Onkologie, Hämatologie und Rheumatologie, Bonn, Deutschland
author Bauer Bauer Claus-Jürgen CJ
Universität Bonn, Uniklinikum Bonn, Medizinische Klinik und Poliklinik III Innere Medizin mit den Schwerpunkten Onkologie, Hämatologie und Rheumatologie, Bonn, Deutschland
author Schäfer Schäfer Valentin Sebastian VS
Universität Bonn, Uniklinikum Bonn, Medizinische Klinik und Poliklinik III Innere Medizin mit den Schwerpunkten Onkologie, Hämatologie und Rheumatologie, Bonn, Deutschland
author German Medical Science GMS Publishing House
Düsseldorf
 610 20260909 engl This is an Open Access article distributed under the terms of the Creative Commons Attribution 4.0 License. Dieser Artikel ist ein Open-Access-Artikel und steht unter den Lizenzbedingungen der Creative Commons Attribution 4.0 License (Namensnennung). M0656 046 Deutsche Gesellschaft für Rheumatologie Deutsche Gesellschaft für Orthopädische Rheumatologie Gesellschaft für Kinder- und Jugendrheumatologie 54. Kongress der Deutschen Gesellschaft für Rheumatologie und Klinische Immunologie (DGRh), 36. Jahrestagung der Gesellschaft für Kinder- und Jugendrheumatologie (GKJR), 40. Jahrestagung der Deutschen Gesellschaft für Orthopädische Rheumatologie (DGORh) Deutscher Rheumatologiekongress 2026 Experimentelle & Translationale Rheumatologie Leipzig 20260909 20260912 ET.22 TextIntroduction: Vascular adhesion protein-1 (VAP-1) is an endothelial cell adhesion molecule possessing enzymatic activity, functioning critically in leukocyte extravasation and vascular inflammation. Its pathophysiological significance in systemic vasculitis including giant cell arteritis (GCA) remains insufficiently characterized. This study aimed to investigate endothelial VAP-1 expression in human aortic endothelial cells (HAoEC), and the immunomodulatory influence of glucocorticoid therapy.Methods: Human aortic endothelial cells (HAoEC) and human umbilical vein endothelial cells (HUVEC, CRL-1730, ATCC) were cultured and stimulated with proinflammatory mediators, including Tumor Necrosis Factor-alpha (TNF-a), Interferon-gamma (IFN-g), and Lipopolysaccharides (LPS), at varying concentrations i.e. 10, 100 µg/mL and time intervals of 24 and 48 hours. Subsequently, VAP-1 surface expression was measured via flow cytometry. The immunomodulatory effect of prednisolone on cytokine induced VAP-1 expression was evaluated in parallel stimulation setups and statistically analyzed.Results: Stimulation of HAoEC cells with proinflammatory mediators induced pronounced VAP-1 expression. TNF-a exhibited the most potent effect, resulting in approximately 80 to 90% VAP-1+ cells at a concentration of 100 µg/mL (p ≤ 0.02). IFN-g and LPS also induced significant upregulation of VAP-1 expression, albeit to a lesser extent than TNF-a. Dose response relationships were observed for all stimuli. Conversely, prednisolone treatment markedly attenuated cytokine induced VAP-1 expression on endothelial cells across all stimulation conditions. Comparison between HAoEC and HUVEC revealed no significant differences in VAP-1 expression under basal or stimulated conditions.Conclusion: This study demonstrated that endothelial VAP-1 expression is induced by proinflammatory stimuli and effectively suppressed by glucocorticoid therapy. Additionally, VAP-1 is significantly upregulated in temporal arteries of patients with GCA. These findings support a functional role for VAP-1 in vascular inflammatory responses and underscore its potential utility as a biomarker and therapeutic target in systemic vasculitis such as GCA.Figure 1 0
1 1 Figure 1: The frequency of VAP-1-positive cells under diverse inflammatory conditions is depicted. Stimulation with Tumor Necrosis Factor-alpha (TNF-a) (p = 0.02), Interferon-gamma (IFN-?), and Lipopolysaccharides (LPS) induced a significant upregulation of expression relative to the unstimulated control.
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