Browsing by Subject "Blebs"

Now showing 1 - 2 of 2
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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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    Etiology of the developing eye in myelencephalic blebs (my) mice
    (Murcia : F. Hernández, 1992) Center, Elizabeth M.; Polizotto, René S.
    The etiology of the eye defects in myelencephalic blebs (my) mutant mice has been poorly understood for almost seventy years. Embryos from 9 to 14 M days of gestation were subjected to Alcian blue 8GX staining for acidic glycosaminoglycan deposition in basement membrane structures of the developing eye in my stock and control specimens. In addition 12 day embryos were subjected to avidinbiotin- peroxidase labelling for laminin. At 9 - 9 M days of gestation more Alcian blue positive extracellular matrix was found in the region between the optic vesicle and the overlying putative lens ectoderm in the my stock embryos. By 12 days, there was an irregular and lesser amount of deposition of glycosaminoglycans in the len's capsule and in the «inner lirniting membrane~ of the presumptive neural retina; however, the deposition of laminin appeared to be greater in the inner lirniting membrane of the my eye. By 14 days, the damage to the eye in the my embryos can be quite extensive, and the deposition of glycosaminoglycans was very meager in this situation. It appears that irregular deposition of glycosaminoglycans in the extracellular matrix and possible increase in the amount of laminin in basement structures in my embryos indicate disruption of the normal histochemistry involved in the development of the eye. Altered histochemistry may in turn indicate changes in permeability between cells of the developing tissues which result in the blebbing.