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Agonistic Antibodies Directed at the Angiotensin II, AT1 Receptor in Preeclampsia

Medical Faculty of the Charité, Franz Volhard Clinic HELIOS Klinikum-Berlin, Berlin; Department of Obstetrics, Charité Campus Virchow, Berlin; Max Delbrück Center for Molecular Medicine, Berlin-Buch, Berlin; Department of Nephrology, Medical School of Hannover, Hannover, Germany; Helios-Clinic, Charité, Campus-Buch, Priv.Doz., Berlin, Germany dechand{at}fvk-berlin.de

Volker Homuth, MD

Gerd Wallukat, PhD

Dominik N. Müller, PhD

Manja Krause, MD

Joachim Dudenhausen, MD

Hermann Haller, MD

Friedrich C. Luft, MD

Medical Faculty of the Charité, Franz Volhard Clinic HELIOS Klinikum-Berlin, Berlin; Department of Obstetrics, Charité Campus Virchow, Berlin; Max Delbrück Center for Molecular Medicine, Berlin-Buch, Berlin; Department of Nephrology, Medical School of Hannover, Hannover, Germany

Immune mechanisms and circulating mediators may be important in the pathogenesis of preeclampsia. We review our findings on agonistic antibodies against the angiotensin II (Aug II) receptor (AT1-AA) and their possible role in the pathogenesis of this disorder. AT1-AA appear in the course of preeclampsia and are largely gone by 6 weeks after delivery. AT1-AA detection relies on a bioassay using spontaneously beating neonatal rat cardiomyocytes. Their specificity has been documented by other methods, including Western blotting, co-localization, and co-immunoprecipitation experiments. AT1-AA induce signaling in vascular cells and trophoblasts including transcription factor activation. The signaling results in tissue factor production and reactive oxygen species generation, both of which have been implicated in preeclampsia. The role of AT1-AA in preeclampsia and other severe hypertensive conditions has not yet been proved with certainty. However, we believe the findings are compelling and warrant further study.

Key Words: Preeclampsia • angiotensin • agonistic autoantibodies • tissue factor • reactive oxygen species

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