2008 NephCure Funded Investigators

Post-Doctoral Fellowship Grants were awarded to:
•    Elizabeth Brown, MD, of the Children’s Hospital Boston, MA
•    Michelle Rheault, MD, of the University of Minnesota, Minneapolis, MN
•    Bart Smeats, PhD, of the Aachen Medical Clinic in Aachen, Germany

Young Investigator Grants were awarded to:
•    Duncan Johnstone, MD, PhD, of the University of Michigan, Ann Arbor, MI
•    Anna Greka, MD, PhD, of Massachusetts General Hospital in Boston, MA
•    Markus Blitzer MD, of the Albert Einstein College of Medicine at Yeshiva University, NY
•    Michael G. Janech, PhD, of Medical University of South Carolina in Charleston, South Carolina

Elizabeth Brown, MD, PhD – Identification of New FSGS Gene: Linkage Mapping of a Large Family
Dr. Brown proposes mapping a novel gene using linkage analysis of a large family with autosomal dominant FSGS to identify a new FSGS causing gene in which initial screening revealed no known mutations in ACTN4 or TRPC6.

Michelle Rheault, MD – The Role of Protein Hic-5 in the Induction of Proteinuria
Dr. Rheault proposes to define the role of hic-5 in mediating enhanced adhesion of potocytes and explore the mechanism by which hic-5 causes proteinuria in hopes to better understand at a molecular level the changes that occur at the potocyte.

Bart Smeets, PhD – Parietal Epithelial Cells, a Regenerative Cell Population
This proposal aims to study the regulation of transdifferentiation of parietal epithelial cells into podocytes. Additionally, Dr. Smeets will test the hypothesis that pharmacological targeting of this process represents a novel approach to renal fibrosis prevention.

Duncan Johnstone, MD, PhD – Interaction of Slit Diaphragm Fat1
The protein Fat1 has a prominent phenotype in the Podocyte, the deletion of which in mice will result in failure to develop normal foot processes. Dr. Johnstone will evaluate the interaction of Fat1 with kinesin, microtubules and actin cytoskeleton.

Anna Greka, MD, PhD – TRPC1 and TRPC5 Channels in Glomerular Podocytes
A mutation in the ion channel TRPC6 was identified as the cause for an autosomal dominant form of familial FSGS. Dr. Greka proposes that dysregulation of TRPC1 and TRPC5, in addition to TRPC6, may play a pathogenic role in FSGS though experiments aimed at molecular and functional characterization of these channels.

Markus Blitzer, MD – The Role of MicroRNAs in Progression of FSGS
Dr. Blitzer has generated an miRNA profile in Albumin/TGF-b1 transgenic mice and found there to be an important role for miR-21 and miR-23b suggesting dysregulation of miRNA is important in podocyte pathology and renal injury. Dr. Blitzer will generate an miRNA s