Helmholtz Gemeinschaft

Search
Browse
Statistics
Feeds

Regulatory antibodies against GPCR in women ten years after early-onset preeclampsia

Item Type:Article
Title:Regulatory antibodies against GPCR in women ten years after early-onset preeclampsia
Creators Name:Birukov, A. and Muijsers, H.E.C. and Heidecke, H. and Drost, J.T. and Cunnigham, M.W. and Kraker, K. and Haase, N. and Frolova, A. and Müller, D.N. and Herse, F. and Maas, A.H.E.M. and Dechend, R.
Abstract:Preeclampsia is associated with an increased cardiovascular risk later in life. Anti-GPCR autoantibodies have been shown to contribute to the development of cardiovascular disease. We investigated whether anti-GPCR autoantibodies are elevated in women with a history of early-onset preeclampsia 8-11 years postpartum, and whether they correlate with clinical outcomes. We investigated data from the Preeclampsia Risk EValuation in FEMales cohort, a retrospective matched case-control study. Anti AT1R-, beta1AR-, ETAR-, PAR1- and CXCR3- autoantibodies were determined in 485 samples by using commercially available ELISA. Women with the lowest combined levels of autoantibodies and a history of early preeclampsia had significantly higher SBP, DBP and MAP (all p<0.001) compared to the controls. The individual titer levels of autoantibodies were not different between controls and former early PE groups 8-11 years postpartum. In conclusion, regulatory autoantibodies alone are not sufficient to explain hypertension or other cardiovascular pathologic conditions, but together with other risk factors such as a previous hypertensive pregnancy, lower levels of autoantibodies are associated with increased blood pressure.
Keywords:Autoantibodies Against GPCR, Preeclampsia, Adverse Pregnancy Outcome, Blood Pressure, Cardiovascular Risk
Source:Frontiers in Bioscience
ISSN:1093-9946
Publisher:Frontiers in Bioscience
Volume:24
Page Range:1462-1476
Date:1 June 2019
Official Publication:https://doi.org/10.2741/4791
PubMed:View item in PubMed

Repository Staff Only: item control page

Open Access
MDC Library