A basic and translational science laboratory focused on diseases of platelets. We are interested in learning the physiologic mechanisms of platelet function, characterizing the genetic variants that can cause inherited platelet dysfunction, and developing therapeutics that can modulate platelet function to ameliorate human disease.

Dr. Williams' research focuses on platelet physiology particularly as it relates to acute coronary syndromes and depression. Her laboratory specifically examines platelet aggregation, flow cytometric analysis to measure platelet activation, platelet luminescence as a measure of the platelet release reaction, many Elisa preparations in order to measure platelet function, platelet genotyping to determine the presence of certain platelet polymorphisms, and various other assays to distinguish mechanisms of platelet dysfunction. The goal for her cardiovascular platelet laboratory is to identify the etiology of platelet dysfunction in many disease states and apply methods that may improve this dysfunction that can eventually be translated to therapies for patients with cardiovascular disease. Scientific techniques performed in the lab include: flow cytometric analysis, platelet microparticle identification, and protein immunoprecipitation among other techniques.

Venous thromboembolism is a major cause of morbidity and mortality. Thrombosis can be caused by acquired or inherited factors, but the genetic contribution to thrombosis is not well defined. Genome wide association studies have recently uncovered new pathways that cause thrombotic disease in humans. The Lowenstein Lab uses human genetics to discover and characterize novel genes that regulate thrombosis and hemostasis. We collaborate with genetic epidemiologists who perform GWAS to identify genetic variants linked to vascular inflammation or thrombosis. We then characterize genetic loci linked to vascular inflammation or thrombosis. These approaches have revealed new pathways in endothelial cells and platelets that contribute to thrombosis and may lead to novel therapies to prevent abnormal bleeding and thrombosis. Current Projects: Genetic causes of venous thromboembolism | Genetic causes of abnormal endothelial activation | Epigenetic regulation of coagulation factor production