In vitro studies of kidney glomerular epithelial cells.

An in vitro model system for studying the glomerular epithelium exposed on the surfaces of kidney slices is described. In the first 12 hours of incubation at 37 degrees C, glomerular podocytes exhibit an increase in number of free surface microprojections and number of cytoplasmic lipid inclusions. During the next several days these cells undergo a series of morphological alterations which resemble a dedifferentiation of the glomerular epithelium. By one week of incubation, the glomerular epithelium has been transformed into a compact group of rounded cells. These cells remain rounded but viable throughout several weeks of subsequent incubation. The glomerular endothelium becomes thickened but also remains viable throughout several weeks of incubation. Surface epithelial cells in both cortical and medullary regions become modified into a thin layer of viable cells. At lower incubation temperatures (e.g. 15 to 33 degrees C), the dedifferentiation of glomerular podocytes and formation of a viable surface layer of cells are significantly inhibited. Both undifferentiated and puromycin aminonucleoside nephrotic glomerular podocytes survive and adapt to the in vitro environment. The in vitro response of glomerular epithelial cells to various compounds added to the incubation media are briefly described. Compounds which induce a loss of cytoplasmic microtubules (e.g. vinblastine, colchicine), cause a loss of podocyte cell body and major process morphological integrity. Neuraminidase removal of the glomerular sialic acid surface coat inhibits the formation of free surface microvilli and results in an early loss of podocyte foot processes. The nephrotoxic agent puromycin aminonucleoside has no effect on the viability or morphology of glomerular cells except at very high concentrations (300 micrograms/ml). The distribution and effects of polycationized ferritin on living glomeruli are briefly described. Finally, in vitro treatment with cytochalasin B appears to inhibit cation-induced loss of podocyte foot processes.