Cell-cycle mechanisms involved in podocyte proliferation in cellular lesion of XXXX .

@entity1 @entity8 @entity8189 @entity628 @entity3808 @entity4910 @entity8985 @entity15308 @entity13525 @entity7596 @entity8755 @entity3969 @entity994
BACKGROUND: Podocyte injury may induce podocyte proliferation, which results in @entity8 . The cellular lesion, seen in some @entity1 with primary @entity628 ( @entity628 ), is characterized by proliferation of cells covering the @entity3808 or collapsed glomerular tufts. Cell-cycle mechanisms by which podocyte proliferation occurs in the cellular lesion of @entity628 are unclear. METHODS: We examined expression patterns of @entity4910 ; cyclin E; @entity7596 ; @entity8189 ; cyclin-dependent kinase ( @entity15308 ; @entity8985 ; such CDK inhibitors as @entity994 ( @entity994 ), @entity13525 ( @entity13525 ), and @entity8755 ( @entity8755 ); and @entity3969 ( @entity3969 ) in 12 renal biopsy specimens with the cellular lesion of @entity628 and 6 renal biopsy specimens with no detectable abnormalities by immunohistochemistry and immunoelectron microscopy. Messenger RNA (mRNA) expression patterns of @entity4910 , cyclin E, @entity994 , @entity13525 , and @entity8755 were evaluated further by in situ hybridization. RESULTS: In controls, immunostaining for @entity7596 , @entity8189 , @entity15308 , @entity8985 , and @entity994 was almost negligible, but positive signals for @entity4910 , cyclin E, @entity13525 , and @entity8755 were observed in glomerular epithelial cells (GECs). In the cellular lesion of @entity628 , positive signals for cyclin E, @entity7596 , @entity8189 , @entity15308 , and @entity994 were present in GEC nuclei, in which @entity3969 , @entity13525 , @entity8755 , and @entity4910 were undetected. Immunoelectron microscopy showed that cyclin E-, @entity15308 -, and @entity994 -specific gold particles were increased significantly in GEC nuclei in the cellular lesion in which cyclin D- and @entity8755 -specific particles were absent compared with controls. An in situ hybridization study showed specific signals of @entity4910 , cyclin E, @entity994 , @entity13525 , and @entity8755 mRNA in GECs forming the cellular lesion of @entity628 . CONCLUSION: Our results suggest that damaged podocytes may inhibit @entity13525 and @entity8755 protein expression, but activate a @entity4910 -independent cell-cycle mechanism and mitotic cell cyclins to promote GEC proliferation in the cellular lesion of @entity628 .
