cofilin-1 inactivation leads to proteinuria – studies in zebrafish, mice and humanscofilin-1失活导致蛋白尿,斑马鱼的研究,老鼠和人类.pdf

Cofilin-1 Inactivation Leads to Proteinuria – Studies in Zebrafish, Mice and Humans 1,3. 2. 2,3 2 2 4 Sharon Ashworth , Beina Teng , Jessica Kaufeld , Emily Miller , Irini Tossidou , Christoph Englert , 2 2,3 5 2 2,3 2,3 Frank Bollig , Lynne Staggs , Ian S. D. Roberts , Joon-Keun Park , Hermann Haller , Mario Schiffer * 1 Department of Biochemistry, Microbiology and Molecular Biology and the School of Biology and Ecology, University of Maine, Orono, Maine, United States of America, 2 Department of Medicine/Nephrology, Hannover Medical School, Hannover, Germany, 3 Mount Desert Island Biological Laboratories, Salsbury Cove, Maine, United States of America, 4 Leibniz Institute for Age Research-Fritz Lipmann Institute e.V. (FLI), Jena, Germany, 5 Department of Cellular Pathology, John Radcliffe Hospital, Oxford, United Kingdom Abstract Background: Podocytes are highly specialized epithelial cells on the visceral side of the glomerulus. Their interdigitating primary and secondary foot processes contain an actin based contractile apparatus that can adjust to changes in the glomerular perfusion pressure. Thus, the dynamic regulation of actin bundles in the foot processes is critical for maintenance of a well functioning glomerular filtration barrier. Since the actin binding protein, cofilin-1, plays a significant role in the regulation of actin dynamics, we examined its role in podocytes to determine the impact of cofilin-1 dysfunction on glomerular filtration. Methods an