Staff Collaborate Conference Room

Debra K. Newman, PhD

Debra Newman, PhD

Debra K. Newman, PhD

Professor, Pharmacology and Toxicology; Senior Investigator at Versiti Blood Research Institute; Adjunct Professor, Microbiology & Immunology

Locations

  • Versiti Blood Research Institute
    Blood Center of Wisconsin

General Interests

Thrombosis, Hemostasis, Immunology and Vascular Biology

Education

PhD, Immunology, Marquette University, 1989

Research Experience

  • Blood Platelets
  • Phosphotyrosine
  • Platelet Activation
  • Platelet Adhesiveness
  • Platelet Aggregation
  • Platelet Endothelial Cell Adhesion Molecule-1
  • Platelet Membrane Glycoproteins
  • Protein Interaction Domains and Motifs
  • Protein Tyrosine Phosphatases
  • Signal Transduction

Research Interests

Platelets are important in early wound healing, where they initially adhere to the extracellular matrix that underlies damaged blood vessels and then aggregate with one another to form a platelet plug. Excessive bleeding occurs when platelet counts are low, or when platelet activity is compromised. Children, especially neonates, who undergo cardiac surgery for repair of congenital heart defects experience excessive bleeding at higher rates than do adults undergoing similar surgeries. We seek to determine the extent to which deficiencies in platelet number or function contribute to excessive bleeding in the setting of pediatric cardiac surgery. This research will help physicians identify pediatric cardiac surgery patients who are at risk for bleeding and administer appropriate blood products in a timely manner should bleeding need to be controlled in this setting.

A major focus of research in our laboratory is Platelet Endothelial Cell Adhesion Molecule-1 (PECAM-1). PECAM-1 is an inhibitory molecule that functions in two important contexts. First, PECAM-1 dampens platelet aggregation in response to low levels of stimulation, which is important to prevent pathological thrombosis. Second, PECAM-1 inhibits T cell responses and interferes with the ability of T cells to kill tumors. We have recently discovered that the ability of PECAM-1 to inhibit T cell anti-tumor responses depends on Transforming Growth Factor β (TGFβ), which is another potent T cell suppressor. Our current work is dedicated to development of a better understanding of how PECAM-1 and TGFβ work together to inhibit T cell responses. This research will help us improve T cell-based therapies for treatment of cancer.

Publications