2009 NephCure Award Recipients NephCure Established Investigator Award Ross Cagan, Ph.D. Mount Sinai School of Medicine A Drosophila model of diabetic nephropathy Dr. Cagan has developed a model of kidney disease using Drosophila (the fruit fly). The fruit fly has cells in its kidneys that are very similar to podocytes, called nephrocytes. By injuring the nephrocytes, Dr. Cagan mimics podocyte injury and searches for ways to repair it. This model allows for the understanding of how podocytes function as well as for the testing of drugs that can reverse podocyte damage. NephCure Young Investigator Award Kirk Campbell, M.D. Mount Sinai School of Medicine, New York, NY Functional characterization of human dendrin mutations in the pathogenesis of FSGS When podocytes become damaged through diseases such as FSGS, proteinuria develops. With enough podocyte loss, patients can progress to ESRD. Dr. Campbell studies FSGS modeled in the mouse and found that the dendrin gene (DDN) is involved in the regulation of the podocyte. He is examining how DDN mutation can lead to the progression of FSGS, and how it regulates podocyte injury and death. This model may lead to the discovery of new approaches that encourage the repair and/or survival of damaged podocytes. NephCure Young Investigator Award Christian Faul, Ph.D. University of Miami, Miami, FL The function of calcineurin in podocytes Calcineurin is a protein that is expressed in all tissues and is inhibited by cyclosporine A (CsA), an immunosuppressant drug sometimes used to treat kidney diseases such as FSGS. Dr. Faul’s research identifies the function of calcineurin in podocytes at the period of transition from early and reversible damage in glomerular disease to late and chronic damage. Examining how ‘signaling’ happens at this transition could serve as a promising target for drug development. Post-Doctoral Fellow Hideki Kato, M.D., Ph.D. Albert Einstein College of Medicine, Bronx, NY The dual role of beta-catenin in podocytes Research indicates that injury to podocytes plays a pivotal role in FSGS disease. Previous studies from Dr. Kato’s laboratory demonstrated that the protein beta-catenin is important in maintaining the structure of the glomerulus. Dr. Kato examined the molecular mechanism that activates beta-catenin to impact the development of proteinuria and glomerular disease. NephCure Young Investigator Award Mira Krendel, Ph.D. SUNY Upstate Medical University, Syracuse, NY The role of myosin 1e-synaptopodin interaction in podocyte functions Complex cells such as podocytes have cytoskeletons that maintain cell structure. Dr. Krendel has found that mutations in myosin 1e, a protein in the cytoskeleton of the podocyte, result in severe defects in the glomerulus. Additionally, myosin 1e interacts with synaptopodin, an important regulator of podocytes. Dr. Krendel hypothesizes that this interaction is involved in regulating the podocyte, and she is examining the mechanism that causes myosin 1e loss and resulting podocyte dysfunction and NS. In addition to examining this interaction at the molecular level, Dr. Krendel is testing the role of myosin 1e and synaptopodin interaction in renal functions in a mouse model. Towards personalized molecular medicine of Nephrotic Syndrome: Transcriptional network analysis to predict treatment response of FSGS. Post-Doctoral Fellow Sebastian Martini, M.D. University of Michigan, Ann Arbor, MI Minimal change disease (MCD), FSGS, and membranous nephropathy (MN) are the primary glomerular diseases associated with NS. The progression of FSGS is often unpredictable and can be difficult to treat leading to ESRD. Dr. Martini is identifying the regulatory pathways, or transcriptional networks, that these diseases might have in common as well as FSGS-specific biomarker ‘signatures’. Identifying which biomarkers differentiate FSGS from the other diseases may potentially be applied to slow disease progression. Young Investigator Award, funded in part by the “Cure for Cole” Fund Valerie Anne Schumacher, Ph.D. Boston Children’s Hospital, Boston, MA Post-transcriptional regulation of gene expression in Glomerular Disease DNA contains the genetic code or instructions needed to build proteins that help make up cells. mRNA translates the DNA into proteins, and each protein has a different function. Most of the inherited forms of NS are caused by mutations in genes that produce proteins critical in podocyte structure. Dr. Schumacher’s research aims to clarify how mutations in the protein WT1 found in the podocyte and how the mechanism of mRNA result in steroid resistant NS that rapidly progresses to FSGS and eventually ESRD. She is studying the generative capability of podocytes to be able to prevent podocyte damage and promote podocyte repair in patients with steroid-resistant NS. NephCure Established Investigator Award Sanja Sever, Ph.D. Massachusetts General Hospital, Boston, MA The role of GTPase dynamin in foot process effacement Podocytes form foot processes that extend into the glomerular filtration barrier. Most forms of NS are characterized by reduction of these extensions and their reorganization, an observation called podocyte ‘foot process effacement’. Dr. Sever’s research focuses on the mechanism that leads to podocyte foot process effacement or reorganization. Additionally, Dr. Sever has found that GTPase dynamin regulates podocytes, and she is examining the molecular mechanism by which dynamin regulates the foot process effacement in order to find new pathways that drugs can target. See Awardees From Other Years: 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2009 2008