Oxidative stress signaling in response to CD4+T cells stimulated via placental ischemia play an important role in hypertension during preeclampsia (860.14)

Abstract

Preeclampsia (PE) is associated with hypertension, oxidative stress, and chronic inflammation. The RUPP rat model of PE and normal pregnant (NP) recipient rats of RUPP CD4+T cells exhibit much of the disease pathology. Reactive oxygen species (ROS) could be released from monocytes or neutropils, however the objective of this study was to determine if RUPP CD4 T cells are a cellular source of ROS and hypertension (MAP) and during pregnancy. CD4+Tcells from RUPP rats were injected into NP recipients on gestational day (GD)13; GD19 MAP, urine and tissues were analyzed. Prior to injection RUPP CD4+ T cells secreted more myleoperoxidase compared to NP (116.9+15.2 vs. 48.5+8.3 ng/mg/mL; p=0.003). Placental NADPH oxidase mediated ROS in RUPP rats was 830.6+68, 726.2+43.73 in NP + RUPP CD4+ T cells and 420.7+51.4 RLU/min/mg in NP rats; p=0.009 and p=0.004, respectively. MAP was 100+2 in NP rats, 126+4 in RUPP rats (p=0.0001) and 118+4mmHg in NP+RUPP CD4+ T cell rats (p=0.002) which was attenuated with apocynin; 111+2 in RUPP + apocynin; 102+3 mmHg in NP + RUPP CD4+ T cells (p=0.01). These data suggest that CD4+Tcells are an important source of ROS mediating hypertension in response to placental ischemia.Grant Funding Source: NIH NICHD; APS STRIDE