Regeneration of sclerosed glomeruli : Mechanism of dedifferentiation and phenotypic changes in podocytes and induce redifferentiation.

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To monitor podocytes derived cells in the pathologic process of glomerular disease, we generate Nephrin-Cre/Rosa26 mice and then we crossed them with p21 deficient mice and induced anti-glomerular antibody glomerulonephritis. The kidney showed marked proteinuria coupled with glomerular epithelial hyperplasia. To analyze the origin and phenotype of these cells, immunohistochemistry for several podocytes markers and incorporation of BrdU was analyzed. Hypercellular lesions were virtually both LacZ and WT1 negative. In addition, we did not find out for LacZ+/WT1-cells or LacZ+/synaptopodin-cells. Thus podocytes dedifferentiation is not occurring in this setting of experimental glomerulonephritis.We are now investigating the plasticity of podocytes focusing on the function of nestin intermediate filament, neurogenic progenitor marker, we found nestin is predominantly expressed in the differentiated podocytes and cytoplasmic distribution of nestin is different from that of actin.siRNA of nestin for immortalized podocytes cell line reveals suppression of process formation suggesting nestin function for podocytes plasticity.