Pre-eclampsia is a disease affecting up to 5% of pregnant women – its key symptoms include high-blood pressure and compromised renal function. In advanced stages, pre-eclampsia can cause placental damage, liver and kidney dysfunction, and cerebral hemorrhaging, which is sometimes fatal for the mother, baby, or both. Previous work demonstrates that autoantibodies from women with pre-eclampsia stimulate AT1 angiotensin receptors, highlighting a possible mechanism for this disease.
To further test this model, Zhou et al. treated mice with IgG from pregnant women with pre-eclampsia and found significant increases in blood pressure and urine protein levels. This effect was prevented by peptide block, or by using antagonists, of the target angiotensin receptor. IgG or affinity-purified AT1 autoantibodies also caused tissue damage in the kidneys and placenta, and smaller fetus sizes. Non-pregnant mice did not show the same physiological responses or kidney damage from IgG treatment, demonstrating that the symptoms were specific to pregnancy. This study establishes a new mouse model for pre-eclampsia and supports screening for angiotensin autoantibodies as an early test for this disease.
