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. Author manuscript; available in PMC: 2012 Jan 20.
Published in final edited form as: J Immunol. 2007 Sep 15;179(6):3391–3395. doi: 10.4049/jimmunol.179.6.3391

FIGURE 1.

FIGURE 1

AT1-AA may underlie many features of preeclampsia by interacting with AT1 receptors on different cell types. AT1-AA from preeclamptic patients function as Ang II in the activation of AT1 receptors at the surface of many cell types. Autoantibody-induced AT1 receptor activation results in increased contraction rates in cardiac myocytes, increased production of NADPH oxidase by trophoblast and vascular smooth muscle cells, PAI-1, sFlt-1, and NADPH oxidase by trophoblast cells, PAI-1 and IL-6 production by mesangial cells, and tissue factor by endothelial cells. AT1-AA-mediated AT1 receptor activation also results in the mobilization of intracellular calcium and the activation of NFAT-responsive genes. We propose that AT1-AA activate AT1 receptors on other cell types, resulting in the physiological changes associated with preeclampsia. Note that increased NADPH oxidase activity leads to increased production of reactive oxygen species (ROS). SMC, Smooth muscle cell; EC, endothelial cell.