PP011. Increased placental expression of angiogenin inhibitor (Ribonuclease inhibitor), a novel gene in pre-eclampsia

Abstract

There is convincing evidence that imbalance between angiogenic and anti-angiogenic factors play an important role in the pathophysiology of pre-eclampsia. Increased expression of soluble fms-like tyrosine kinase-1 (sFlt1), along with decreased placental growth factor (PlGF) and vascular endothelial growth factor (VEGF) appear to play a key role in the abnormal placentation and vascular dysfunction of pre-eclampsia. Angiogenin is a potent inducer of angiogenesis and serum levels are elevated in pre-eclampsia. Angiogenin Inhibitor (also called placental Ribonuclease inhibitor) is a potent antagonist of both angiogenic and ribonucloetic activities of angiogenin. We demonstrate that placental expression of angiogenin inhibitor is altered in pre-eclampsia and may play a role in its pathophysiology. The aim of the study was to assess the expression of angiogenin inhibitor in healthy normotensive and pre-eclamptic placentas. Placental expression of angiogenin inhibitor was measured in term placentae of 14 pre-eclamptic women and 16 normal pregnant controls. The women were matched for age, gestation and parity. Placental tissue was collected immediately after delivery and stored at -80°C. The angiogenin inhibitor gene expression was measured using real-time quantitative polymerase chain reaction (rt-QPCR). The results were standardized using the glyceraldehyde-3-phosphate dehydrogenase (GAPDH) reference gene. mRNA expression of angiogenin inhibitor gene was significantly increased in pre-eclamptic placentae (p=0.027) compared to normal pregnant controls; 0.44 (0.174-1.048) versus 0.091 (0.029-0.301), median and interquartile range, for pre-eclampsia and normal controls, respectively. Placenta expression of angiogenin inhibitor gene is significantly increased in pre-eclampsia and may play a role in its pathophysiology. This finding may directly correlate with the reported ability of angiogenin inhibitor to protect from oxidative stress by its reactivity as an oxygen species scavenger.