Our efforts on fundamental research focus on the regulation of microvascular exchange function. The process of cell life depends on adequate exchange of solutes across microvascular walls. However, the exact steps between activation of the signaling pathways and the increase in permeability at the cellular and molecular levels remain to be elucidated. We have shown that PKC and eNOS interact to promote a hyperpermeability state in response to substances such as platelet-activating factor and vascular endothelial growth factor. Our current goals are to define the role of eNOS signaling in the regulation of vascular permeability in health and disease, and identify the function of eNOS translocation as a signaling mechanism in vivo.

At the clinically relevant front, we study the pathophysiologic molecular basis of vascular diseases such as chronic venous insufficiency, inflammation, ischemia-reperfusion injury, and diabetes mellitus. Our research on chronic venous insufficiency derives from the medical and socio-economic impact of the disease. We conduct our studies using human dermal fibroblasts and immortal cell lines to determine the underlying cellular pathologies. In particular, we investigate the regulatory role of TGF-ß1 and extracellular proteins on the genesis of venous ulcers. Similarly, diabetes mellitus is a disease that affects over 25% of the population and leads to vascular disease. We aim to elucidate the signaling pathways that cause endothelial cells to become dysfunctional after exposure to excessive glucose or lack of insulin.

We use computer-assisted video image digital analysis, intravital fluorescence microscopy, western blotting, and RT-PCR methods in these investigations.