Acute Kidney Injury and Kidney Fibrosis
Dr. Al-Bataineh's Research
My current research focuses primarily on studying the acute and chronic effects of the cell surface protein mucin 1 (Muc1) in regulating the b-catenin pathway during moderate and severe ischemia-reperfusion injury (IRI) in a mouse model.
Dr. Hughey's Research
Research in my laboratory is focused on characterization of the assembly, processing and membrane trafficking of apically expressed glycoproteins in polarized kidney epithelial cells. We use biochemistry and electrophysiology techniques in cultured cells and Xenopus oocytes, as well as transgenic mice, to study the function of glycosylation, palmitoylation and proteolytic processing of model proteins such as the epithelial sodium channel (ENaC), gamma-glutamyltranspeptidase and the cell surface sensor MUC1. Our recent studies have revealed that ENaC is activated by a very novel mechanism of proteolytic release of inhibitory peptides both in the biosynthetic pathway and post-Golgi compartments, and in pathological states such as proteinuria (kidney) and Cystic Fibrosis (lung). Our current studies of MUC1 function in normal kidney epithelia are focused on its role in epithelial survival and recovery from acute kidney injury using both a model of polarized kidney epithelial cells cultured under hypoxic conditions, and a proven mouse model of kidney ischemia-reperfusion injury.
Dr. Tan's Research
I am interested in unraveling the molecular mechanisms underlying the development of chronic kidney disease and fibrosis utilizing both in vivo and in vitro approaches. In particular we are assessing novel ways in which the glomerular and tubular compartment cross-talk in disease, and how the Nrf2/Keap1 pathway can be leveraged to prevent CKD. We also study how the Wnt/beta-catenin pathway and matrix metalloproteinases affect renal injury.
Division of Renal-Electrolyte Academic Offices
A919 Scaife Hall
3550 Terrace Street
Pittsburgh, PA 15261