Richard D. Minshall, Ph.D. (Professor, Anesthesiology Pharmacology, Bioengineering) studies the molecular regulation of endothelial permeability pathways and pathological mechanisms of pulmonary hypertension, acute lung injury, and ARDS. In addition, Minshall and colleagues are investigating anti-inflammatory, immunomodulatory, and anti-metastatic effects of volatile and local anesthetics.
Project 1. The specific roles of ICAM-1, Src, eNOS, and caveolin-1 regulated signaling in endothelial cells, isolated lungs, and whole animals are being studied with regards to normal lung physiology and disease mechanisms. Dr. Minshall is an internationally recognized expert in caveloin-1 and signaling in lung endothelial cells. Caveolin-1 is a multi-functional protein required for caveolae formation and transendothelial transport and thus plays a critical role in lung microvascular endothelial cell barrier regulation and drug delivery. He has published several sentinel papers on caveolin-1 regulation of endothelial cell function via downstream associated Src and eNOS signaling pathways, and the roles of oxidative stress signals in endothelial hyperperpermeability and inflammatory syndromes. The focus of his current work is to understand how caveolin-regulated endothelial cell signaling mechanisms regulate caveolae formation and trafficking dynamics, cell-cell communication, PMN adhesion, and endothelial and epithelial cell proliferation and differentiation as critical components of lung vascular and airway development, permeability regulation, inflammatory injury, and repair/remodeling. Drs. Minshall, Hu and Dull collaborate on projects related to acute lung injury, regulation of endothelial permeability and the role of eNOS in sepsis and mechanotransduction.
Project 2. Dr. Minshall and Dr. Votta-Velis (Anesthesiology) are investigating the molecular actions of local anesthetics as anti-metastatic agents. In ongoing studies, they are focused on understanding effects of local anesthetics on ICAM-1, Src, and eNOS signaling in vascular endothelial cells.