Roxanna Irani, a M.D./Ph.D. student at The University of Texas Graduate School of Biomedical Sciences at Houston (GSBS), has received a $10,000 fellowship for her efforts to better understand a condition known as pre-eclampsia that threatens the lives of expectant women and their unborn children.
The fellowship was awarded through the new Jess Hay Endowment for Chancellor's Graduate Student Research Fellowships, which supports graduate student research fellowship grants to students attending any of the UT institutions. Named after the former chairman of The University of Texas System Board of Regents, the endowment "ties timely graduate education to timely and high-quality research, which benefits the state," said Randa Safady, Ph.D., vice chancellor for external relations at UT System.
Pre-eclampsia affects millions of women worldwide every year and is responsible for about 15 percent of early deliveries in North America. It typically occurs late in pregnancy and is associated with a sudden increase in blood pressure, kidney damage and swelling of the hands, feet and face. Because the cause of this serious disease is unknown, the current treatment is limited to the delivery of the baby and placenta. Pre-eclampsia can be a fatal condition and leads to 18 percent of pregnancy-related maternal deaths annually in the United States.
Irani was a co-author on a 2008 study in Nature Medicine in which researchers induced pre-eclampsia in pregnant mice by injecting them with autoantibodies isolated from women with the condition. Unlike antibodies that help the body fight off infection, autoantibodies attack their own cells.
Building on this research, which suggests that pre-eclampsia is an autoimmune disorder, Irani studied the impact of pre-eclampsia on the fetuses of pregnant mice and tested different drugs and proteins, which block the features of pre-eclampsia in pregnant mice. A manuscript on her recent findings will be published in the Nov. 23 print edition of The Journal of Experimental Medicine.
"Our pre-clinical research demonstrates that exposure to this autoantibody during development can lead to smaller fetuses, which suffer from kidney and liver defects. When we block the effects of the autoantibody in the mouse model, the size of the babies is restored and the placental and organ damage are lessened," Irani said.