Our laboratory is broadly interested in the biology of calcium signaling.  Thousands of calcium channels on the cell’s plasma membrane precisely control the timing and entry of calcium ions. Calcium permeates the membrane of virtually every cell to mediate vital processes such as contraction, vesicle secretion, gene transcription, and programmed cell death, to name a few.  We are particularly interested in the role of calcium in the regulation of the actin cytoskeleton. Aberrant calcium signaling leading to a disrupted cytoskeleton has been linked to neurologic disorders, heart disease, cancer, and kidney disease. 

Our current efforts are focused on Transient Receptor Potential channels (TRP) as regulators of actin dynamics and cell motility in glomerular podocytes, fibroblasts and neurons.  We recently uncovered TRPC5 and TRPC6 as the calcium influx pathways regulating the activity of the RhoGTPases Rac1 and RhoA, respectively. 

Our current efforts are also directed toward understanding the role of TRPC channels in proteinuric kidney disease. We recently revealed that TRPC-mediated Rho GTPase signaling may cause podocyte injury. These findings have implications for severe kidney diseases such as Nephrotic Syndrome, including Minimal Change Disease, Focal and Segmental Glomerulosclerosis and Membranous Nephropathy, to name a few. Our data also reveal TRPC channels as the target of upstream receptor pathways such as the Angiotensin Receptor. Thus, TRPC channels may also be novel targets for anti-proteinuric therapies in acquired proteinuric disease such as hypertensive and/or diabetic nephropathy.

We are using the tools of molecular biology, cell biology, advanced imaging techniques, patch clamp electrophysiology and animal models to study the role of TRP channels in health and disease.