Glycosaminoglycans of the plasma membranes of renal tubule and liver cells

Lis, Dora; Monis, Benito

doi:10.1002/jss.400120103

Cited by 5 publications

(4 citation statements)

References 40 publications

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“…5) might play a pivotal role in the multistep process of liver cell damage (36) or, in the Initiation of cell division following injury (37). Both assumptions arise from the previously discussed (28) and above briefly mentioned physiological functions of pericellular proteoheparan sulfate (6,(9)(10)(11)(12). In addition to the key role of changes of the plasmalemma in the pathogenesis of toxic liver injury (38)(39)(40)(41) structural alterations of the glycocalyx may have importance for Under the protective effects of diethyldithiOcarbamate (42) and of the natural flavonoid (*)cianidanol-3 (43-45) on the development of galactosainine-hepar titis, a less pronoünced Inhibition of proteogiycan synthesis was observed.…”

Section: Discussionmentioning

confidence: 99%

“…Heparan sulfate, the preponderant type of glycosaminoglycan in liver (7,8) occurs predominantly in the microenvironment of the cell, i.e. the external surface of the hepatocyte (6,(9)(10)(11)(12) and piay there control the exchange of metabolites, ions, fluids, and wateir, exert some effects on hepatocellular proliferation and may regulate the accessibility of cell surface receptors (13-15). The physiological significance of the galactosamine containing sulfated glycosaminoglycans (chondroitin sulfate, dermatan sulfate) in liver is not known.…”

Section: Introductionmentioning

confidence: 99%

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The Sequence of Changes in the Biosynthesis of Sulfated Glycosaminoglycans in Acute, Experimental Liver Disease

Gressner¹,

Heinrigs²,

Grouls³

1982

CCLM

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The incorporation of [ 35 S]sulfate into total and specific glycosaminoglycans of the liver of rats injured acutely by a singie intraperitoneal dose of either jD-galactosamine (700 and 350 mg/kg body weight, respectively) or thioacetamide (100 mg/kg body weight) was studied in vivo and in liver slices. Regardless of the chemical nature of the hepatotoxic agent and its mechanism of action the incorporation of isotope in vivo is changed biphasically: a rapidly occurring and strong Inhibition is followed by pronounced elevation in later stages of injury. In contrast to the dose-dependent Inhibition of heparan sulfate formation the production of chondroitin sulfate and dermatan sulfate is only slightly and for a rather short period of time diminished. The synthesis of the latter glycosaminoglycans is stimulated 3 to 4 fold 8 to 24 h after onset of liver damage, fhat of heparan sulfate about 2 fold. Impaired synthesis of heparan sulfate occurs before the elevation of the activities of aspartate aminotransferase, alanine aminotransferase, and leucine arylamidase in serum. The specific radioactivity of 3'-phosphoadenosine-5'-phosphosulfate remains nearly constant in galactosamine-damaged livers. Similar time-dependent changes of [ 3S S]sulfate incorporation into heparan sulfate, chondroitin sulfate and dermatan sulfate were measured in slices from livers injured in vivo for various times with -D-galactosamine or thioacetamide. Neither serum from normal nor galactosaniine-treated rats influences the total amount and the pattern of glycosaminoglycans synthesized in normal or injured liver slices. Hepatic glycosaminoglycan formation of 3.5 and 33 months old rats responds quantitatively and qualitatively in a simüar way to £>-galactosamine; 50% Inhibition is reached with about 80 mg/kg of the hepatotoxin. The Inhibition of heparan sulfate synthesis in early injured livers could not be reversed by addition of p-nitrophenyl-/3-Z)-xylopyranoside to the medium (final concentration l mmol/1), but in rats treated with diethyldithiocarbamate or the flavonoid (+)-cianidanol-3, prior to injection of Z)-galactosamine, a partial restoration of the diminished synthesis of total glycosaminoglycans and of heparan sulfate is achieved. Die Sequenz der Änderungen der Biosynthese sulfatierter Glykosaminoglykane bei akuten, experimentellen LebererkrankungenZusammenfassung: Der Einbau von [ 3 *S]Sulfat in die gesamten und spezifischen Glykosaminoglykane der Leber von Ratten, die akut geschädigt wurden durch eine intraperitoneale Einzelinjektion von entweder Z)-Galaktosamin (700 mg/kg oder 350 mg/kg Körpergewicht) oder Thioacetamid (100 mg/kg), wurde in vivo und in Leberschnitten untersucht. Ungeachtet der chemischen Natur der hepatotoxischen Substanz und ihres Wirkungsmechanismus kommt es zu einer biphasischen Änderung des Isotopeinbaues: eine unmittelbar auftretende und starke Hemmung wird gefolgt von einer ausgeprägten Erhöhung in späteren Stadien der Schädigung. Im Gegensatz zu der dosisabhängigen Hemmung der Heparansulfatbildung ist die Pr...

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The Sequence of Changes in the Biosynthesis of Sulfated Glycosaminoglycans in Acute, Experimental Liver Disease

Gressner¹,

Heinrigs²,

Grouls³

1982

CCLM

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“…The luminal surface of the distal nephron has a glycocalyx composed of glycosaminoglycans as well as other proteins that are set in a hydrated polysaccharide gel (43,44,61,65,96,97,109,126). Glycosaminoglycans consist of negatively charged disaccharide repeats that are linked to core proteins.…”

Section: Sensing Flow In Principal and Intercalated Cellsmentioning

confidence: 99%

Regulation of cation transport in the distal nephron by mechanical forces

Satlin¹,

Carattino²,

Liu³

et al. 2006

American Journal of Physiology-Renal Physiology

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Thiazide and loop diuretics induce renal K(+) secretion, often leading to renal K(+) wasting and hypokalemia. This phenomenon has been proposed to reflect an increase in delivery to and reabsorption of Na(+) by the distal nephron, with a resultant increase in the driving force for passive K(+) efflux across the apical membrane. Recent studies suggest that cellular mechanisms that lead to enhanced rates of Na(+) reabsorption as well as K(+) secretion in response to increases tubular flow rates are more complex. Increases in tubular flow rates directly enhance the activity of apical membrane Na(+) channels and indirectly activate a class of K(+) channels, referred to as maxi-K, that are functionally inactive under low flow states. This review addresses the role of biomechanical forces, generated by variations in urinary flow rate and tubular fluid volume, in the regulation of transepithelial Na(+) and K(+) transport in the distal nephron. The question of why the distal nephron has evolved to include a component of flow-dependent K(+) secretion is also addressed.

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“…Glycosaminoglycans are main constituents of the intercellular matrix in tissues such äs cartilage, skin and cornea (4) but are also present in parenchymatous organs like liver (6), brain (7,8), and kidney (9,10). In the latter type of tissues glycosaminoglycans are also distributed intracellularly (10,12) and pericellularly (9,13,14).…”

Section: Introductionmentioning

confidence: 99%

Laser Nephelometric Determination of Glycosaminoglycans — Method and Application

Gressner¹,

Scherer²,

Stuhlsatz³

1983

Clinical Chemistry and Laboratory Medicine

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Light scattering due to the formation of insoluble complexes between the long-chain quaternary ammonium sah N-cetylpyridinium chloride and glycosaminoglycans was utilized for a relative simple, sensitive and precise determination of total and specific types of glycosaminoglycans by laser nephelometry. The addition of the ammonium salt to Solutions of various glycosaminoglycans in 0.03 mol/1 NaCl produces a time-dependent increase in light scattering, which reaches a maximum between 14 and 18h of complex formation, irrespective of the type of glycosaminoglycan studied. Only keratan sulphate does not generate light scattering, and is therefore not detectable by the procedure. The scattering of laser light by certain types of sulphated glycosaminoglycans (e.g. heparan sulphate, heparin) depends more on the degree of sulphation (charge density) than on chain length within a certain ränge. Optimum light scattering was found at 28 mmol/l N-cetylpyridinium chloride and at a ionic strength around 0.03 mol/1 NaCl.The detection limits and linear ranges of the individual glycosaminoglycans were evaluated. For the determination of chondroitin sulphate, laser nephelometry is at least 8 times more sensitive and much more simple than the modified carbazole method (glucuronic acid). The intra-assay and inter-assay coefficients of Variation are about 4% and 7%, respectively. Laser nephelometry is much more sensitive than turbidimetry. Complex synthetic mixtures of glycosaminoglycans and biological fluids were accurately differentiated by successive chemical and enzymatic degradation of the respective glycosaminoglycans followed by the measurement of the resulting reduction of laser light scattering. In synovial fluids from non-inflammatory joint diseases, light scattering (units/ml) was about 4.5 times higher than in synovial fluids from inflammatory articular lesions. In both pathologic conditions nearly all of the light scattering can be attributed to hyaluronic acid.

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Glycosaminoglycans of the plasma membranes of renal tubule and liver cells

Cited by 5 publications

References 40 publications

The Sequence of Changes in the Biosynthesis of Sulfated Glycosaminoglycans in Acute, Experimental Liver Disease

The Sequence of Changes in the Biosynthesis of Sulfated Glycosaminoglycans in Acute, Experimental Liver Disease

Regulation of cation transport in the distal nephron by mechanical forces

Laser Nephelometric Determination of Glycosaminoglycans — Method and Application

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