Glomerular handling of circulating glycated albumin in the normal mouse kidney

Londono, Irène; Ghitescu, Lucian; Bendayan, M.

doi:10.1152/ajprenal.1995.268.5.f913

Cited by 12 publications

(31 citation statements)

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“…These changes became more important along with the duration of the hyperglycaemic state. For the glomerular permselectivity, the molecular conformation of the basement membrane matrix and the concentrations of glycation of circulating proteins are assumed to be responsible for the restricted passage of serum proteins [64]. Changes in these characteristics lead to alterations in permeability properties [64].…”

Section: Discussionmentioning

confidence: 99%

“…For the glomerular permselectivity, the molecular conformation of the basement membrane matrix and the concentrations of glycation of circulating proteins are assumed to be responsible for the restricted passage of serum proteins [64]. Changes in these characteristics lead to alterations in permeability properties [64]. Diabetes or prolonged periods of hyperglycaemia do affect drastically the glycation of proteins, glomerular basement membrane integrity and its filtration properties [15,18,25,27,28].…”

Section: Discussionmentioning

confidence: 99%

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Morpho-functional studies of the blood-brain barrier in streptozotocin-induced diabetic rats

Bouchard

Bendayan

2002

Diabetologia

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Aims/hypothesis. We undertook the characterization of the capillary bed of the rat frontal cortex and their permeability properties in short-term and long-term diabetic rats. Methods. Diabetes was induced by strepozotocin injection. Rats were maintained hyperglycaemic without insulin treatment during 4 to 5 months (short-term) and 8 to 13 months (long-term). Rats from an additional short-term hyperglycaemic group received an injection of exogenous dinitrophenylated albumin 15 min before being killed. Tissues were processed for electron microscopy and quantitative immunocytochemistry. Endogenous and dinitrophenylated exogenous albumin were revealed with high resolution over the capillary wall using specific antibodies and the protein A-gold complex. Morphometrical analyses were carried out. Results. Albumin is transported across endothelial cells by plasmalemmal vesicles or caveolae and larger vacuolar structures. This transport increased in diabetic rats by an increment in the number of vesicles. Albumin distribution across the capillary basement membrane showed that the restrictive properties of the basement membrane present in normoglycaemic rats are altered in the diabetic condition, as was its thickness. Similar alterations of the basement membrane structure and function were encountered in old normoglycaemic rats but to a lesser extent. Conclusion/interpretation. The results indicate that diabetes seems to accelerate the ageing process of the vascular wall and that the central nervous system capillary bed is also a target for diabetic microangiopathy.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Morpho-functional studies of the blood-brain barrier in streptozotocin-induced diabetic rats

Bouchard

Bendayan

2002

Diabetologia

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“…2). However, it is well documented that dinitrophenylation induces few changes in albumin conformation (Kessler et al, 1982;Londoñ o et al, 1995) and that DNP-BSA carrying less than 10 DNP residues per molecule is cleared from circulation at a rate virtually identical to that of the native albumin (Kitteringham et al, 1985). Only a relatively small percentage (less than 8% as assessed by densitometry) of the tracer was found as a dimer, whereas the majority of DNP-BSA was in a monomeric form, even after storage at high concentrations.…”

Section: Characterization Of the Tracermentioning

confidence: 99%

Alterations of the Rat Mesentery Vasculature in Experimental Diabetes

Arshi

Bendayan

Ghitescu

2000

Laboratory Investigation

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SUMMARY:The alteration induced by diabetes on vascular permeability to serum albumin was investigated in the mesentery of streptozotocin-induced hyperglycemic rats. Double-tagged ( 125 I and dinitrophenol-haptenated) heterologous albumin was intravenously administered in normal and hyperglycemic animals, and the extravasation of the tracer was evaluated by radioactivity measurements and by morphometry at the ultrastructural level using quantitative protein A-colloidal gold immunocytochemistry. The results demonstrate that diabetes induces a significant increase in the permeability of the mesentery vessels to albumin. This increase is due to a more efficient transport of macromolecules by endothelial plasmalemmal vesicles and not to leakier interendothelial junctions. Passage across the endothelial basement membranes did not appear to be restricted in either the control or diabetic condition. However, in diabetes, the mesothelial basement membrane appeared to become modified and to restrain the passage of albumin toward the peritoneal cavity. After 3 months of diabetes, the rats presented a net increase in the average diameter of the blood vessels localized in the mesentery arcada (macrovascular hyperplasy) and a notable angiogenesis, manifested at the level of the microvasculature in the mesenteric windows. (Lab Invest 2000, 80:1171-1184.T he association of diabetes with vascular dysfunctions gradually evolving toward incapacitating or life-threatening vascular pathologies is undisputed. Extensive clinical observations and studies on animal models have amply documented that hyperglycemia accelerates and worsens atherosclerosis in large arteries (Colwell et al, 1988;Shantaram, 1999;Steiner 1997) and affects, although in different ways, the microvessels of selected vascular beds, such as those of the retina (Bazan et al, 1997;Cunha-Vaz, 1983;Porta, 1996;Ruggiero et al, 1997), kidney (Flyvbjerg, 1997;Mauer et al, 1984;Nyengaard and Bendtsen, 1993;Vlassara et al, 1994), and nerves (Cameron and Cotter, 1997;Malik et al, 1993; Tesfay et al, 1994). Particular attention has been directed to the study of diabetes-induced retinopathies and nephropathies, because of their obvious clinical implications. On the other hand, the impact of diabetes on other vascular beds has been generally overlooked. Therefore, it is not known whether diabetic microangiopathy concerns all blood vessels, creating a sort of "dysfunctional background" exacerbated in particular tissues by local factors to a full blown vascular pathology, or the vasculature of many organs is simply spared by the deleterious effects of hyperglycemia/ hypoinsulinemia. The latter hypothesis would fall in line with the ever-growing body of evidence pointing to important physiological and biochemical dissimilarities between various vascular segments (Boegehold, 1998;Rajotte et al, 1998;Thorin and Shreeve, 1998).Several morphologic features and physiologic parameters appear as leit motifs of diabetic microangiopathies. Among these, the thickening of the basement membran...

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“…It is known that a substantial amount of albumin is filtered through the glomeruli to the proximal tubular lumen; however, a very small fraction of the filtered albumin is excreted in the final urine, and proximal tubular cells reabsorb a large part of filtered albumin [20, 21, 22]. Renal proximal tubular cells are known to absorb modified albumin by endocytosis through the apical membrane [13, 23].…”

Section: Discussionmentioning

confidence: 99%

Renal Proximal Tubular Metabolism of Protein-Linked Pentosidine, an Advanced Glycation End Product

Asano¹,

Fujita²,

Ueda

et al. 2002

Nephron

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Background: Pentosidine, an advanced glycation end product, accumulates in plasma proteins of uremic patients. Its fate is, however, yet to be fully understood. Methods: Three cell lines, JTC-12 (proximal tubular cells), MDCK (distal tubular cells), and BALB3T3 (nonrenal cells), were cultured in a double chamber system and were exposed to uremic serum, and the contents of protein-linked pentosidine derived from uremic sera were determined in each medium by HPLC assay. The presence of pentosidine in the cytoplasm of these cells was assessed by immunoperoxidase staining. Results: When the apical cell membrane was exposed to uremic serum (fortified in the upper chamber), the contents of protein-linked pentosidine in the upper medium decreased by up to 30% after 24- and 48-hour incubations of JTC-12 cells but not of other cells. On the other hand, the contents of protein-linked pentosidine in the lower medium did not change. By contrast, exposure of the basolateral cell membrane of the three cell lines to uremic serum (fortified in the lower chamber) did not change the contents of protein-linked pentosidine both in the upper and lower medium after a 24-hour incubation. Pentosidine was detected immunohistochemically in the cytoplasm of JTC-12 cells, but not of BALB3T3 and MDCK cells, the apical membranes of which were exposed to uremic sera for 8 h. The immunoreaction disappeared 48 h after exposure. Pentosidine was not detected in the cytoplasm of JTC-12 cells, the basolateral membranes of which were exposed to uremic sera. The relevance of the in vitro results to humans was demonstrated by immunohistochemical studies in normal human kidney tissues showing that pentosidine was identified in the proximal renal tubules. Conclusion: These results suggest that the proximal tubular cells play a role in the disposal of plasma pentosidine.

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Glomerular handling of circulating glycated albumin in the normal mouse kidney

Cited by 12 publications

References 0 publications

Morpho-functional studies of the blood-brain barrier in streptozotocin-induced diabetic rats

Morpho-functional studies of the blood-brain barrier in streptozotocin-induced diabetic rats

Alterations of the Rat Mesentery Vasculature in Experimental Diabetes

Renal Proximal Tubular Metabolism of Protein-Linked Pentosidine, an Advanced Glycation End Product

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