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(American Journal of Pathology. 2004;164:1417-1424.)
© 2004 American Society for Investigative Pathology

Differential Expression of D-Type Cyclins in Podocytes in Vitro and in Vivo

Arndt Petermann*, Keiju Hiromura{dagger}, Jeffrey Pippin{dagger}, Mary Blonski{dagger}, William G. Couser{dagger}, Jeffrey Kopp{ddagger}, Peter Mundel§ and Stuart J. Shankland{dagger}

From the Universitätsklinikum RWTH Aachen,* Aachen, Germany; Department of Medicine,{dagger} Division of Nephrology, University of Washington School of Medicine, Seattle, Washington; the National Institutes of Health,{ddagger} Bethesda, Maryland; and the Departments of Medicine and Anatomy,§ Albert Einstein College of Medicine, Bronx, New York

The proliferative response of podocytes to injury determines the histological phenotype. Moreover, an apparent lack of podocyte proliferation may underlie the development of glomerulosclerosis. Podocyte proliferation is closely linked with its state of differentiation. However, the mechanisms regulating these processes are not fully elucidated. Because D-type cyclins have been shown to be important in the regulation of proliferation and differentiation, we examined their expression in podocytes in vitro and in vivo. The glomerular expression of cyclins D1 and D3 was examined in vitro in cultured immortalized podocytes by immunostaining and Western blot analysis, and in embryonic mice and rats, the passive Heymann nephritis model of experimental membranous nephropathy in rats, and human immunodeficiency virus (HIV)-transgenic mice. Kidneys from cyclin D1 knockout mice were also examined. Cyclin D1 was abundant in cultured proliferating podocytes, but not in quiescent differentiated podocytes. In contrast, cyclin D3 was abundant in differentiated, but not proliferating podocytes. Cyclin D1 was expressed in embryonic mouse and rat glomeruli during the S- and comma-shaped stages, and was absent in podocytes at the capillary loop stage and in mature rodent glomeruli. Cyclin D1 protein increased after injury in passive Heymann nephritis rats and in HIV-transgenic mice. Cyclin D3 was constitutively and specifically expressed in podocytes in normal rodent glomeruli, and decreases during dedifferentiation and proliferation in HIV-transgenic mice. Kidneys from cyclin D1-/- mice were normal with the podocytes expressing specific differentiation markers. Cyclin D1 is not necessary for the terminal differentiation of podocytes, and expression coincides with cell-cycle entry. In contrast, cyclin D3 expression coincides with podocyte differentiation and quiescence.




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