Effects and molecular mechanisms of AT1-AA in retinopathy of preeclampsia

Abstract

Preeclampsia not only seriously endangers maternal and fetal health during pregnancy but may incur many sequelae in postpartum women such as reduced visual acuity. Agonistic autoantibodies to the angiotensin II type I receptor (AT1-AA) is closely associated with preeclampsia. The aim of the present study is to determine whether AT1-AA is associated with retinal impairment during the course of preeclampsia. A preeclampsia model was established by injecting AT1-AA into pregnant rats via the tail vein. Changes in the retinal histological structure were observed. Cell apoptosis and cytokines including reactive oxygen species (ROS), as well as apoptosis-related proteins such as Bcl-2, Bax, and caspase-3 were detected. In addition, flash electroretinograms obtained at different postpartum days were analyzed. Compared with the control group, the retinal structure became edematous and the cell density was reduced significantly in preeclampsia group. The cell apoptosis rate was increased significantly. In addition, the content of ROS, the levels of Bax and caspase-3 in the retina were increased, while the content of Bcl-2 was reduced significantly. Continuous observation of the electroretinograms showed loss of retinal ganglion cells postpartum. The present study demonstrated that AT1-AA induced retinal cell apoptosis by promoting ROS release and activating caspase, suggesting that the increased postpartum susceptibility of preeclamptic women to retinopathy is related to AT1-AA-induced cell apoptosis.