Our Research

Research in the McDonald Laboratory is examining the cellular mechanisms of angiogenesis, vascular remodeling, and lymphangiogenesis in mouse models of cancer and chronic inflammation. Our research uses in-vivo cell-biological approaches to determine how abnormalities of blood vessels and lymphatics contribute to disease pathophysiology.

Current interests include the mechanisms of preventing, stopping, or reversing disease-related changes in the vasculature and the consequences of these actions. Related interests are the regulation of endothelial barrier function, downstream effects of altered plasma leakage and cellular trafficking, and control mechanisms of tissue fluid and cell clearance by lymphatics.

Projects in the laboratory are using mouse models to dissect the roles of growth factors and receptors involved in growth and remodeling of blood vessels and lymphatics and related processes. The actions of VEGF, VEGF-C, angiopoietins, PDGF, TNF-alpha, cMET, and FAK are among them. Signaling is manipulated in vivo by switchable transgenic overexpression, genetic deletion, viral vectors, or pharmacological agonists or inhibitors.

Ongoing studies are using the models to examine mechanisms that drive or modify remodeling of blood vessels and lymphatics in inflammatory conditions, with an emphasis on the airways and lungs. Other studies are elucidating favorable and unfavorable effects of destroying blood vessels in tumors, reflected by tumor growth, invasion, and metastasis.

The overall direction is to understand mechanisms of stopping or reversing angiogenesis and lymphangiogenesis and the downstream benefits and other consequences of manipulating blood vessels and lymphatics in cancer and chronic inflammation.