Basement membrane charge in human glomerular disease

1986 ◽  
Vol 150 (4) ◽  
pp. 267-278 ◽  
Author(s):  
Peter N. Furness ◽  
David R. Turner ◽  
Roger E. Cotton
2010 ◽  
Vol 298 (3) ◽  
pp. F702-F711 ◽  
Author(s):  
Takamoto Ohse ◽  
Michael R. Vaughan ◽  
Jeffrey B. Kopp ◽  
Ronald D. Krofft ◽  
Caroline B. Marshall ◽  
...  

Studies have shown that certain cells of the glomerular tuft begin to express proteins considered unique to other cell types upon injury. Little is known about the response of parietal epithelial cells (PEC) to injury. To determine whether PECs change their phenotype upon injury to also express proteins traditionally considered podocyte specific, the following four models of glomerular disease were studied: the transforming growth factor (TGF)-β1 transgenic mouse model of global glomerulosclerosis, the adriamycin model of focal segmental glomerulosclerosis (FSGS), the anti-glomerular basement membrane (GBM) model of crescentic glomerulonephritis, and the passive Heymann nephritis model of membranous nephropathy. Double immunostaining was performed with antibodies to podocyte-specific proteins (synaptopodin and Wilms' tumor 1) and antibodies to PEC specific proteins (paired box gene 8 and claudin-1). No double staining was detected in normal mice. In contrast, the results showed a statistical increase in the number of cells attached to Bowman basement membrane that were double-positive for both podocyte/PEC proteins in TGF-β;1 transgenic, anti-GBM, and membranous animals. Double-positive cells for both podocyte and PEC proteins were also statistically increased in the glomerular tuft in TGF-β1 transgenic, anti-GBM, and FSGS mice. These results are consistent with glomerular cells coexpressing podocyte and PEC proteins in experimental glomerular disease, but not under normal circumstances.


Author(s):  
Rachel Lennon ◽  
Neil Turner

The glomerular basement membrane (GBM) is a condensed network of extracellular matrix molecules which provides a scaffold and niche to support the function of the overlying glomerular cells. Within the glomerulus, the GBM separates the fenestrated endothelial cells, which line capillary walls from the epithelial cells or podocytes, which cover the outer aspect of the capillaries. In common with basement membranes throughout the body, the GBM contains core components including collagen IV, laminins, nidogens, and heparan sulphate proteoglycans. However, specific isoforms of these proteins are required to maintain the integrity of the glomerular filtration barrier.Across the spectrum of glomerular disease there is alteration in glomerular extracellular matrix (ECM) and a number of histological patterns are recognized. The GBM can be thickened, expanded, split, and irregular; the mesangial matrix may be expanded and glomerulosclerosis represents a widespread accumulation of ECM proteins associated with loss of glomerular function. Whilst histological patterns may follow a sequence or provide diagnostic clues, there remains limited understanding about the mechanisms of ECM regulation and how this tight control is lost in glomerular disease. Monogenic disorders of the GBM including Alport and Pierson syndromes have highlighted the importance of both collagen IV and laminin isoforms and these observations provide important insights into mechanisms of glomerular disease.


1981 ◽  
Vol 18 (6_suppl) ◽  
pp. 6-22 ◽  
Author(s):  
Peter M. Burkholder

A captive colony of galagos that for several years lived under poor housing conditions and suffered a variety of chronic illnesses showed a high incidence of renal glomerular disease. Several patterns of glomerular disease were seen: four types of proliferative lesions included a mild stalk glomerulitis, more severe stalk-lobular proliferative glomerulonephritis, diffuse proliferative glomerulonephritis, and diffuse proliferative and sclerotic glomerulonephritis; and a form of glomerular capillary basement membrane thickening. Glomerular localization of immunoglobulin and the third component of complement as well as some unusual ultrastructural observations in diffuse proliferative and sclerotic glomerulonephritis suggest an immunopathogenesis for this disease.


2012 ◽  
Vol 160 (4) ◽  
pp. 291-297 ◽  
Author(s):  
Ying Maggie Chen ◽  
Jeffrey H. Miner

2007 ◽  
Vol 171 (1) ◽  
pp. 139-152 ◽  
Author(s):  
Scott J. Harvey ◽  
George Jarad ◽  
Jeanette Cunningham ◽  
Angelique L. Rops ◽  
Johan van der Vlag ◽  
...  

2008 ◽  
Vol 173 (4) ◽  
pp. 927-937 ◽  
Author(s):  
Rosa M. Baleato ◽  
Petrina L. Guthrie ◽  
Marie-Claire Gubler ◽  
Leonie K. Ashman ◽  
Séverine Roselli

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