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Cell-cycle regulatory proteins in podocyte cell in idiopathic nephrotic syndrome of childhood. Background. The podocyte cell is believed to play an important role in idiopathic nephrotic syndrome (INS) of childhood. In adults with cellular and collapsing focal segmental glomerulosclerosis (FSGS), the expression of cell-cycle regulatory proteins such as p27, p57, and cyclin D is decreased and expression of cyclin A, Ki-67, and p21 is observed in podocyte cells suggestive of a dysregulated podocyte phenotype. We investigated for alterations in the expression of cyclin kinase inhibitors, p27, p57, p21, and cyclins D and A in the podocyte cell of children with INS. Methods. Forty-two kidney biopsies were investigated; 14 with minimal-change disease (MCD), seven with diffuse mesangial hypercellularity (DMH), 12 with FSGS, four with Alport syndrome (AS), and five normal biopsies. The sections were examined by immunohistochemistry using dual staining method. Podocyte cells were first identified by Wilm's tumor-1 staining after which expressions of cell-cycle regulatory proteins were analyzed. A quantitative analysis was performed for the proportion of podocyte cells that expressed each cell cycle regulatory protein. Results. On light microscopy, all podocyte cells expressed p27, while p57 and p21 expression was seen in a portion of podocyte cells in normal kidney biopsies. Cyclin D was expressed in a small percent of podocyte cells though the expression was more marked in mesangial and endothelial cells. Cyclin A expression was not seen in normal biopsies. The mean expression of p27 decreased significantly in order from normal (100%), MCD (45.9%), DMH (22.4%), and FSGS (16.7%), and the difference between MCD and FSGS was significant. p21 was significantly and equally reduced in MCD (2.3%), DMH (0%), and FSGS (0.7%) compared to normal (66.6%). There was no significant difference in expression of p57, cyclin D and cyclin A in the podocyte cells between normal and... [ABSTRACT FROM AUTHOR]

Analyzes the expression of synaptopodin in childhood idiopathic nephrotic syndrome. Association of synaptopodin with actin microfilaments; Response of synaptopodin to podocyte cells; Disaggregation of actin cytoskeleton.