Rashmi Sood, PhD
Assistant Professor of Pathology
Dr. Rashmi Sood received her PhD in Molecular Biology from the Tata Institute of Fundamental Research, University of Bombay, India. Her postdoctoral studies were conducted at the Blood Research Institute, Blood Center of Wisconsin, Milwaukee, where she specialized in coagulation and vascular biology. Dr. Sood’s laboratory develops and utilizes rodent models of placental disease and pregnancy disorder to understand disease mechanisms. In parallel, her laboratory seeks to discover predictive biomarkers that can be used to identify high-risk pregnancies in women.
- Maternal/fetal health
- Coagulation and platelet disorders
- Placental disorders and hypertensive disorders of pregnancy
- Estrogen-coagulation cross-talk
- Biomarkers of pregnancy complications
- Assistant Professor, Department of Pathology, Medical College of Wisconsin (2008-present)
- Investigator, Division of Pathology, Children’s Research Institute (2008-present)
- Assistant Professor, Department of Cell, Biology, Neurobiology & Anatomy, Medical College of Wisconsin (2013-present)
- University of Delhi, India – Bachelor of Science (1983)
- University of Delhi, India – Master of Science (1985)
- Tata Institute of Fundamental Research, University of Bombay – PhD (1999)
- Blood Research Institute, Blood Center of Wisconsin, Milwaukee, WI – Postdoctoral Fellow (2000-2002)
- National Institutes of Health, Award # 1 R01 HL112873-01A1
- American Heart Association, Scientist Development Grant #0930200N
- March of Dimes Foundation, Basil O’ Connor Starter Scholar Award #5-FY09-120
Research in the Sood laboratory is focused on issues related to women’s health and pregnancy. Pregnancy is an intimate relationship between the mother and the fetus. The placenta serves as an essential organ to coordinate this relationship. Suboptimal placental function compromises fetal growth and puts the baby at risk for adult-onset metabolic and cardiovascular disorders. Adverse consequences for the mother include hypertensive disorders of pregnancy, such as preeclampsia. These conditions affect 5 to 8% of all pregnancies.
A developing fetus relies on the placenta for nutrition and other essential functions. To perform these functions, the human placenta forms unusual vascular spaces filled with maternal blood and directly accessible to placental cells. Such vascular spaces are atypical and not found anywhere else in the human body. It is unclear how blood flow is maintained in these vascular spaces and what leads to pathological thrombosis. One focus of our research is to test the current paradigms of coagulation and platelet biology in the context of placental development and utero-placental circulation. Using microarray-based technology, we have shown that placental trophoblast cells express a repertoire of molecules with anticoagulant and anti-platelet activities, suggesting that they are active participants in the local regulation of blood clotting. We hypothesized that maternal and fetal factors coordinately regulate hemostasis at the feto-maternal interface. This hypothesis was proven to be true in studies with mice where combining maternal and fetal thrombophilia mutations resulted in placental failure and fetal loss. Further work with this murine model has demonstrated that placental failure is mediated by low level thrombin generation and the activation of maternal platelets, yet involves a platelet function other than the formation of blood clots. Treatment of the mother with heparin allows placental development to proceed and affords significant protection, but the therapeutic effect of heparin is not replicated by anticoagulation with other agents including fondaparinux. Ongoing studies investigate molecular details of platelet recruitment to the placenta and the mechanisms by which platelets disrupt placental function. We also investigate the mechanism of heparin’s ability to improve placental health. These studies lay the groundwork to develop informed therapeutic approaches to placental disease caused or aggravated by activated coagulation.