Dissemin is shutting down on January 1st, 2025

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Public Library of Science, PLoS ONE, 6(8), p. e65887, 2013

DOI: 10.1371/journal.pone.0065887

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Celiac Disease–Specific TG2-Targeted Autoantibodies Inhibit Angiogenesis Ex Vivo and In Vivo in Mice by Interfering with Endothelial Cell Dynamics

Journal article published in 2013 by Suvi Kalliokoski, Biokémikus) Szondy Zsuzsanna (1959-) (molekuláris sejtbiológus, Ana-Marija Sulic, Korponay-Szabó Ilma (1959-) (gyermekgyógyász), Ilma R. Korponay-Szabó, Zsuzsa Szondy, Rafael Frias, Mileidys-Alea Perez, Stefania Martucciello ORCID, Anne Roivainen, Lauri J. Pelliniemi, Carla Esposito, Martin Griffin, Daniele Sblattero, Markku Mäki and other authors.
This paper is made freely available by the publisher.
This paper is made freely available by the publisher.

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Abstract

Public Library of Science open access ; A characteristic feature of celiac disease is the presence of circulating autoantibodies targeted against transglutaminase 2 (TG2), reputed to have a function in angiogenesis. In this study we investigated whether TG2-specific autoantibodies derived from celiac patients inhibit angiogenesis in both ex vivo and in vivo models and sought to clarify the mechanism behind this phenomenon. We used the ex vivo murine aorta-ring and the in vivo mouse matrigel-plug assays to address aforementioned issues. We found angiogenesis to be impaired as a result of celiac disease antibody supplementation in both systems. Our results also showed the dynamics of endothelial cells was affected in the presence of celiac antibodies. In the in vivo angiogenesis assays, the vessels formed were able to transport blood despite impairment of functionality after treatment with celiac autoantibodies, as revealed by positron emission tomography. We conclude that celiac autoantibodies inhibit angiogenesis ex vivo and in vivo and impair vascular functionality. Our data suggest that the anti-angiogenic mechanism of the celiac disease-specific autoantibodies involves extracellular TG2 and inhibited endothelial cell mobility