Modulation of cytoskeletal organization of podocytes during the course of aminonucleoside nephrosis in rats

By immunoelectron microscopy the modulation of cytoskeletal organization of podocytes during the course of puromycin aminonucleoside‐induced nephrosis was examined. In control rats, tubulin and vimentin were present, limited to the podocyte cell body and the major processes. Their distribution in the foot processes was virtually negative. Myosin exhibited the same distribution pattern, albeit much more scattered, with no relation to any podocyte organelles or cell structures. Actin was scattered over the fibrillar zones of the cell body and its processes, including the foot processes. In proteinuric rats, loss of foot processes occurred and the glomerular basement membrane was covered by broad cytoplasmic sheets of podocytes, which contained these four subunits of cytoplasmic filaments. Accompanied by the disappearance of proteinuria, the structural organization of the foot processes was completely restored, in which tubulin, vimentin, and myosin were scarcely observed. Our results confirmed that the loss of foot processes is caused by their retraction, and indicated that the specific localization of the podocytic cytoskeleton contributes to the maintenance of the particular cell shape. Its reorganization may account for the structural modification of podocytes.

[1]  C. Whiteside,et al.  Podocytic cytoskeletal disaggregation and basement-membrane detachment in puromycin aminonucleoside nephrosis. , 1993, The American journal of pathology.

[2]  C. Alpers,et al.  Markers of complement-dependent and complement-independent glomerular visceral epithelial cell injury in vivo. Expression of antiadhesive proteins and cytoskeletal changes. , 1992, Laboratory investigation; a journal of technical methods and pathology.

[3]  D. Lovett,et al.  Mesangial cell activation by bacterial endotoxin. Induction of rapid cytoskeletal reorganization and gene expression. , 1991, The American journal of pathology.

[4]  K. Kawasaki,et al.  Variable expression of desmin in rat glomerular epithelial cells. , 1990, The American journal of pathology.

[5]  C. Whiteside,et al.  Glomerular epithelial detachment, not reduced charge density, correlates with proteinuria in adriamycin and puromycin nephrosis. , 1989, Laboratory investigation; a journal of technical methods and pathology.

[6]  R. Franke,et al.  Ultrastructural organization of contractile and cytoskeletal proteins in glomerular podocytes of chicken, rat, and man. , 1988, Laboratory investigation; a journal of technical methods and pathology.

[7]  Y. Kanwar,et al.  Effect of beta-D-xyloside on the renal glomerular cells. II. Morphological studies. , 1987, Laboratory investigation; a journal of technical methods and pathology.

[8]  P. Andrews,et al.  Filamentous actin bundles in the kidney , 1984, The Anatomical record.

[9]  G. Feldmann,et al.  Cytoskeleton ultrastructure of podocytes and glomerular endothelial cells in man and in the rat , 1984, The Anatomical record.

[10]  R. Albrecht,et al.  Platelet activation and cytoskeletal reorganization: high voltage electron microscopic examination of intact and Triton-extracted whole mounts , 1984, The Journal of cell biology.

[11]  Y. Kanwar,et al.  Altered glomerular permeability as a result of focal detachment of the visceral epithelium. , 1982, Kidney international.

[12]  P. Andrews.  Investigations of cytoplasmic contractile and cytoskeletal elements in the kidney glomerulus. , 1981, Kidney international.

[13]  D. Kerjaschki.  Polycation-induced dislocation of slit diaphragms and formation of cell junctions in rat kidney glomeruli: the effects of low temperature, divalent cations, colchicine, and cytochalasin B. , 1978, Laboratory investigation; a journal of technical methods and pathology.

[14]  P. Andrews.  The effect of vinblastine-induced microtubule loss on kidney podocyte morphology. , 1977, The American journal of anatomy.

[15]  M. Karnovsky,et al.  An ultrastructural study of the mechanisms of proteinuria in aminonucleoside nephrosis. , 1975, Kidney international.

[16]  O. H. Griffith,et al.  The molecular reorganization of lipid bilayers by osmium tetroxide. A spin-label study of orientation and restricted y-axis anisotropic motion in model membrane systems. , 1973, Archives of biochemistry and biophysics.

[17]  P. McMillan,et al.  Preservation of erythrocyte ghost ultrastructure achieved by various fixatives. , 1973, Proceedings of the National Academy of Sciences of the United States of America.

[18]  R. Bulger,et al.  Effect of vinblastine sulfate on the fine structure of cells of the rat renal corpuscle. , 1972, The American journal of anatomy.

[19]  M. Arakawa,et al.  A scanning electron microscope study of the glomerulus. Further consideration of the mechanism of the fusion of podocyte terminal processes in nephrotic rats. , 1972, Laboratory investigation; a journal of technical methods and pathology.

[20]  D. Pease.  Myoid features of renal corpuscles and tubules , 1968 .

[21]  Trump Bf,et al.  Electron microscopic studies of human renal disease. Observations of normal visceral glomerular epithelium and its modification in disease. , 1962 .

[22]  M. Bendayan,et al.  Contractile proteins in podocytes: immunocytochemical localization of actin and alpha-actinin in normal and nephrotic rat kidneys , 1991, Virchows Archiv. B, Cell pathology including molecular pathology.

[23]  T D Pollard,et al.  Actin and actin-binding proteins. A critical evaluation of mechanisms and functions. , 1986, Annual review of biochemistry.

[24]  F. Chatelanat,et al.  ULTRASTRUCTURE OF THE NORMAL AND PATHOLOGICAL GLOMERULUS , 1969 .