Abstract 036: Regulation of sFlt-1 Splicing by U2AF and JMJD [Session Title: Pregnancy and Preeclampsia]

Preeclampsia (PE) is a gestational disorder defined by new-onset hypertension and maternal endothelial dysfunction. Though its origins are unclear, placental ischemia is thought to be the central cause. In response, the placenta releases pathogenic factors, such as the anti-angiogenic soluble form of the VEGF receptor Flt-1 (sFlt-1), into the maternal circulation. sFlt-1 is a soluble splice variant of the VEGF receptor Flt-1, acting as a VEGF sink in the circulation. The regulation of sFlt-1 splicing is not completely understood, but it is proposed that the splicing factor U2AF65 promotes splicing, while JMJD6 opposes it by degrading U2AF65. Here, we test the hypothesis that decreased expression of U2AF65 will decrease sFlt-1 release, while decreased JMJD6 will increase sFlt-1 release. Using immortalized placental trophoblasts (BeWo), siRNA was used to knock down the expression of U2AF65, confirmed by RT-qPCR (1.014 + 0.12 vs 0.379 + 0.131; p

Source: Hypertension - September 14, 2017 Category: Cardiology Authors: Adrian C Eddy, Heather Chapman, Eric M George Tags: Oral Abstract Presentations Source Type: research