Tanya Mayadas


Research Area



Our laboratory is interested in understanding mechanisms of inflammation focusing both on the molecular basis of neutrophil recruitment, activation and function in autoimmune mediated diseases, and the endothelial dependent pathways regulating vascular permeability to macromolecules.

An inflammatory response requires the recruitment of innate immune cells (e.g. neutrophils and monocytes) through their interaction with the endothelium, followed by the induction of processes that allow them to engulf targets, release proteinases and generate reactive oxygen species to eliminate the offending stimuli. This innate immune response is critical for host defense but also contributes to tissue injury associated with inflammatory diseases. A major interest of the laboratory is to elucidate the neutrophil dependent mechanisms of tissue injury in autoimmune diseases such as glomerulonephritis, and the contribution of adhesion receptors and associated signaling pathways in regulating the activation and function of this cell type.  Related to our interest in glomerulonephritis, which is a leading cause of renal failure worldwide, we aim to understand the role of two TNF receptors, TNFR1 and TNFR2 on the endothelium, in the pathogenesis of IgG immune complex mediated glomerulonephritis.

In addition to our interest in leukocyte biology, our research has a strong vascular biology focus. Vascular permeability permits the passage of small molecules required for maintaining tissue fluid homeostasis. An increase in permeability is a hallmark of inflammation, and hyperpermeability and loss of endothelial barrier function is associated with many diseases from acute respiratory distress syndrome to diabetes and cancer. We study mechanisms of cAMP dependent regulation of endothelial cell junction remodeling, a dynamic process that controls vascular integrity, permeability and cell migration. We aim to determine how cAMP induced activation of Epac1, a cAMP responsive guanine exchange factor for Rap GTPases markedly increases basal endothelial barrier function and counteracts leakage induced by permeability inducing agents. In particular, we focus on delineating the role of Epac1, Rap GTPases, A-kinase anchoring protein-9 (AKAP9) and microtubule dynamics in this p

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