Presenting Author
University of Mississippi Medical Center
As an Early Stage Investigator (ESI), I am currently launching my independent clinical and basic research program in the pathogenesis and treatment of the pregnancy-specific hypertensive disorder, preeclampsia (PE). I am Assistant Professor at University of Mississippi Medical Center (UMMC), and my passion is to translate my basic science work into human health through clinical trials. There is no known cure and the only effective treatment is delivery of the fetus and placenta. PE affects 5-7% of all pregnancies in the U.S., and is associated with reduced placental perfusion and fetal weight, increased inflammation, antiangiogenic factor sFlt-1, vascular endothelial dysfunction and hypertension. Despite being a leading cause of maternal death and perinatal morbidity, the mechanisms responsible for the pathogenesis of PE still are unclear. As a graduate student, I received funding support from ‘Conselho Nacional de Desenvolvimento Científico e Técnológico’ (CNPq/Brazil) during my Master degree in pharmacology to conduct clinical research in gestational hypertension and preeclampsia. As a Ph.D. student, I received a predoctoral fellowship from ‘Fundação de Amparo à Pesquisa de São Paulo’ (FAPESP/Brazil) to conduct clinical and animals studies in PE and I was able to learn and work with the placental ischemic rat model of preeclampsia, induced by long-term reductions in uterine perfusion pressure (RUPP model). During my fellowship tenure, I used RUPP rat PE model to assess nitric oxide synthase (NOS) expression, nitric oxide bioavailability, oxidative stress and vascular reactivity in response to placental ischemia. In 2013, as a postdoctoral fellow at University of Mississippi Medical Center-UMMC, I have continued to work in the RUPP rat as well as other unique rat models of preeclampsia produced by increased cytokine expression, CD4+ T helper cell adoptive transfer or AT1-AA infusion in order to determine the beneficial effects of adding 17-OHPC to the clinical management of preterm PE for mother and child. Moreover, I have helped students and fellows with the design and performance of experiments, plotting and critical analysis of results, and writing and revision of manuscripts. In 2016, I was successful at obtaining Pharmaceutical AMAG-LUMARA investigator initiated grant to support my travel and supplies for additional projects related efficacy of progesterone in severe preterm preeclampsia. My work is reflected on my extensive publication record as an early stage investigator: 55 articles (11 as first author papers, 2 senior papers and 1 under preparation, 42 co-authorships) and 70 peer-reviewed abstracts published in esteemed scientific journals. Relevant for this poster presentation, my laboratory has shown that PE is a progesterone deficient state that is associated with an imbalance between TH1/TH2 cells, natural killer (NK) cells, and inflammatory cytokines which in turn lead to endothelial dysfunction, uterine growth restriction and high blood pressure. In contrast, healthy normal pregnancy (NP) is associated with elevations in progesterone and TH2/uterine NK cells favoring immunotolerance of the fetus. Activated lymphocytes during normal pregnancy express progesterone receptors, which stimulate a protein called Progesterone Induced Blocking Factor (PIBF). PIBF increases during NP and has been shown to bind IL-4 receptor and stimulate IL-4/TH2 cells, both of which are reduced during PE. The role of PIBF in PE still unknown, however I believe that levels of PIBF are low in PE patients that exhibit lower circulating progesterone compared to normal pregnant patients. In 2018, I was a recipient of the NIH/ NIGMS Pilot project grant which has provided me support and preliminary data to obtain my 2019 Career Development Award, American Heart Association. Indeed, I recent received a pilot grant from the NIGMS Mississippi Center for Clinical and Translational Research (MCCTR) which has provided me support for my independent preliminary data presented is this poster.