Browsing by Subject "Renal corpuscle"

Now showing 1 - 3 of 3
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    Acidic glycosaminoglycans and laminin-1 in
    (Murcia : F. Hernández, 1997) Center, Elizabeth M.; Emery, K.E.
    Deposition of glycosaminoglycans and laminin-1 in the renal corpuscles of the kidneys of mylencephalic blebs, 'blebs', (my) and normal C57BLl 65 mice was compared in embryonic, neonatal (newbom to approximately two days old) and adult animals. Utilization of Alcian Blue 8GX staining, at a pH of 2.5, revealed an increase in acidic glycosaminoglycans in the parietal layer of Bowman's capsule and in general, an increase in the mesangial matrix of the glomerulus of my mutant adults. An increase in glycosaminoglycans was also noted in the developing kidney in certain my embryos in tissues associated with the glomeruli, but no significant differences were observed between the kidneys of neonatai my and control mice. The laminin-1 procedure revealed more deposition of laminin in the basement membrane of the parietal layer of Bowman's capsule in the neonatal and adult mutant my mice. Altered deposition of basement membrane and extracellular matrix components may reflect changes in the pattern of development and in the functioning of the kidney. Morphological changes in the human kidney are associated with alteration of function; a similar association may be occurring in the mice homozygous for the my gene.
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    HGSNAT enzyme deficiency results in accumulation of heparan sulfate in podocytes and basement membranes
    (Universidad de Murcia, Departamento de Biologia Celular e Histiologia, 2019) Nagel, Lauren; Oliveira, Regiana; Pshezhetsky, Alexey V.; Morales, Carlos R.
    ucopolysaccharidosis III type C is a lysosomal storage disorder caused by the accumulation of heparan sulfate in lysosomes. The disorder occurs due to Heparan Acetyl-CoA: α-glucosaminide N- acetyltransferase (HGSNAT) deficiency, an enzyme which typically catalyzes the transmembrane acetylation of heparan sulfate, a basement membrane component. When the gene encoding this enzyme is mutated, it cannot perform the processing of heparan sulfate, leading to un-acetylated heparan sulfate build-up in the lysosomes of cells, causing a storage disorder. This defect has been studied primarily in brain and liver cells, but its effect on the structural integrity of the glomerulus is poorly known. The present study focuses on the effect of Hgsnat gene inactivation and heparan sulfate toxicity on the integrity of the renal corpuscle. This cortical structure was chosen because of its abundance of basement membranes and heparan sulfate as well as the renal corpuscle’s physiological importance in glomerular filtration. Light microscopy, electron microscopy, and immunocytochemistry of genetically modified mice revealed a buildup of lysosomes in the podocytes, suggesting that these cells are responsible for the processing of glomerular basement membranes
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    Ultrastructure of the renal corpuscle of Testudo graeca Chelonia. A comparison between hibernating and non-hibernating animals.
    (Murcia : F. Hernández, 1986) Zuasti, A.; Ferrer, C.; Ballesta Germán, José; Pastor García, Luis Miguel
    The renal corpuscle of hibernating and nonhibernating Testudo graeca was studied by means of light and electron microscopy. Renal corpuscles are small and have a glomerular architecture similar to that found in other vertebrates with a limited glomerular filtration rate. In hibernating animals, unlike non-hibernating, some n~orphologicacl hanges took place. The cells of the renal corpuscle were densely packed, podocytes and parietal cells bhowed a marked cytoplasmic vacuolization, there was a highly developed capillary basement membrane and the endothelial and mesangial cells showed abundant dense granules. These morphological features apparently correspond to a vacuolar degeneration. They may also be the morphological basis of the decrease in the glomerular filtration rate observed during this period.