Distribution of intermediate filament proteins in normal and diseased human glomeruli

• Published in: The American journal of pathology Vol. 125; no. 3; pp. 465 - 475
• Main Authors: Stamenkovic, I, Skalli, O, Gabbiani, G
• Format: Journal Article
• Language: English
• Published: Bethesda, MD ASIP 01.12.1986; American Society for Investigative Pathology
• Subjects: Animals; Biological and medical sciences; Desmin - metabolism; Female; Fibronectins - immunology; Fluorescent Antibody Technique; Glomerulonephritis; Glomerulonephritis - metabolism; Humans; Intermediate Filament Proteins - metabolism; Keratins - metabolism; Kidney Glomerulus - metabolism; Medical sciences; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Rats; Vimentin - metabolism; Renal glomerulus; Human; Glomerulonephritis; Proteins; Vertebrata; Mammalia; Urinary system disease; Rat; Rodentia; Immunofluorescence
• ISSN: 0002-9440; 1525-2191

The distribution of intermediate filament proteins (vimentin, desmin, and cytokeratin) was studied by means of immunofluorescence in the normal human and rat glomerulus and in pathologic human glomeruli. Antifibronectin antibodies were used as mesangial markers. In normal human glomeruli, vimentin antibodies stained endothelial cells, podocytes, and mesangial cells; desmin antibodies, surprisingly, stained podocytes. In normal rat glomeruli, the pattern of vimentin staining was the same as in humans, but desmin antibodies stained both mesangial cells and podocytes. In human and rat glomeruli cytokeratin staining was confined to segments of Bowman's capsule. In human pathologic glomeruli, vimentin and desmin antibodies stained the structures that were positive in normal glomeruli, giving a characteristic pattern for each pathologic condition examined. These results are compatible with the mesenchymal origin of podocytes and mesangial cells and suggest that both cells have smooth muscle-like phenotypic features. Mesangial cells may have slightly different differentiation paths in humans and rats, leading to a distinct expression of intermediate filament proteins.