Research Interests

My long-term research interest is in understanding the interplay between cellular signaling and membrane trafficking.

In this respect, endothelial cells (cells that line the interior surface of blood vessels) are convenient and important model to study. Endothelium is involved in control of blood pressure and inflammation, and endothelial dysfunction is associated with such diseases as atherosclerosis and pulmonary edema. Cell-cell junctions hold endothelial cells joined together, so that they efficiently separate blood from the underlying tissues, forming an endothelial barrier. Upon injury or infection, thrombin, one of the major inflammatory factors, acts through G-protein coupled receptors and activates several heterotrimeric G-proteins. This induces release of a content of Weibel-Palade bodies (secretory granules), which promotes platelet adhesion and aggregation and mediates vascular inflammation. To allow passage of leukocytes from the bloodstream to a site of inflammation, protein complexes of cell-cell junctions need to be temporarily reorganized, which requires both exo- and endocytotic pathways.

Using multidisciplinary approach we established a direct interaction of G{alpha}12 and {alpha}SNAP, an intrinsic component of membrane fusion machinery, and suggested that this interaction may regulate the presence of VE-cadherin on the cell surface / adherens junctions and therefore endothelial barrier function. Further exploration should shed light on which of the multiple transport pathways (exocytosis of newly synthesized proteins, endocytosis followed by degradation or recycling to the site of cell-cell contact) may be affected by the G{alpha}12-{alpha}SNAP interaction.

G-protein mediated signal transduction involved in membrane trafficking will remain in focus of my further research.