Sialic acid-containing glycoproteins on renal cells determine nucleation of calcium oxalate dihydrate crystals

Lieske, John C.; Toback, F. Gary; Deganello, Sérgio

doi:10.1046/j.1523-1755.2001.00015.x

Cited by 52 publications

(45 citation statements)

References 13 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…[21][22][23] Moreover, these proteins have been reported to also have some calcification promoter activity because of their heterogeneous nucleant capacity. [24][25][26] It appears that the major calcification modulator role of these proteins is as regulators of osteoclast/osteoblast cell activity. 7,8,27 Crystallization inhibitors obstruct or prevent crystal development.…”

mentioning

confidence: 99%

Effect of Crystallization Inhibitors on Vascular Calcifications Induced by Vitamin D A Pilot Study in Sprague-Dawley Rats

Gráses

Sanchís

Perelló

et al. 2007

Circ J

View full text Add to dashboard Cite

mentioning

confidence: 99%

Effect of Crystallization Inhibitors on Vascular Calcifications Induced by Vitamin D A Pilot Study in Sprague-Dawley Rats

Gráses

Sanchís

Perelló

et al. 2007

Circ J

View full text Add to dashboard Cite

“…Therefore, we and others have hypothesized that attachment of newly formed crystals to the tubular cell surface (5-10) and the cellular responses that follow (11)(12)(13) could result in crystal retention and thereby set in motion a series of events that lead to pathologic renal calcification. Adhesion of calcium oxalate crystals to anionic, sialic acid-containing molecules on the surface of renal epithelial cells is crystal-face specific (14) and can be blocked by competing soluble anions in tubular fluid such as glycosaminoglycans, citrate, or glycoproteins (5,6). Exposure of cells to agents that raise intracellular cAMP, including prostaglandin E 2 , (PGE 2 ), decreases cellular affinity for crystals, whereas blockade of PGE production enhances it (15).…”

mentioning

confidence: 99%

Modulation of Proliferating Renal Epithelial Cell Affinity for Calcium Oxalate Monohydrate Crystals

Farell¹,

Huang

Kim

et al. 2004

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Abstract. Adhesion of urinary crystals to distal tubular cells could be a critical event that triggers a cascade of responses ending in kidney stone formation. Monolayer cultures of distal nephronderived MDCKI cells were used as a model to study crystal-cell interactions. COM crystal adhesion reached a peak 2 d after plating and progressively fell thereafter. The decline in crystal binding was accelerated by prostaglandin E 2 (PGE 2 ) supplementation and delayed by blockade of PG production. Crystals avidly adhered to cells that migrated in to repair a scrape wound made in the monolayer and after a transient hypoglycemic insult. Exposure of MDCKI cells to uric acid crystals and soluble uric acid was also associated with increased crystal adhesion. Treatment of physically or hypoglycemically injured cells with trypsin or neuraminidase reduced crystal binding to baseline levels, suggesting that increased exposure of cell surface glycoproteins mediated the effect, whereas PGE 2 treatment blunted crystal binding to regenerating cells. Furthermore, when cells were grown in the presence of synthetic D-mannosamine analogues that can modify the conformation of cell surface sialoglycoconjugates, crystal binding to proliferating cells was decreased, whereas blockade of N-

show abstract

“…Uric acid crystal binding did not depend on anionic cell surface binding molecules (79). CaOx dihydrate (COD) nucleated directly on the cell surface via their [101] face (80), to become associated with the membrane through their [100] face (81,82). Crystal binding stimulated additional crystal attachment and was inhibited by arachidonic acid or other compounds that raise intracellular cAMP (83).…”

Section: Crystal-cell Interactionsmentioning

confidence: 99%

Crystal Retention in Renal Stone Disease

Verkoelen¹

2006

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

The mechanisms that are involved in renal stone disease are not entirely clear. In this article, the various concepts that have been proposed during the past century are reviewed briefly and integrated into current insights. Much attention is dedicated to hyaluronan (HA), an extremely large glycosaminoglycan that may play a central role in renal stone disease. The precipitation of poorly soluble calcium salts (crystal formation) in the kidney is the inevitable consequence of producing concentrated urine. HA is a major constituent of the extracellular matrix in the renal medullary interstitium and the pericellular matrix of mitogen/stress-activated renal tubular cells. HA is an excellent crystal-binding molecule because of its size, negative ionic charge, and ability to form hydrated gel-like matrices. Crystal binding to HA leads to crystal retention in the renal tubules (nephrocalcinosis) and to the formation of calcified plaques in the renal interstitium (Randall's plaques). It remains to be determined whether one or both forms of renal crystal retention are involved in the development of kidney stones (nephrolithiasis).

show abstract

Sialic acid-containing glycoproteins on renal cells determine nucleation of calcium oxalate dihydrate crystals

Cited by 52 publications

References 13 publications

Effect of Crystallization Inhibitors on Vascular Calcifications Induced by Vitamin D A Pilot Study in Sprague-Dawley Rats

Effect of Crystallization Inhibitors on Vascular Calcifications Induced by Vitamin D A Pilot Study in Sprague-Dawley Rats

Modulation of Proliferating Renal Epithelial Cell Affinity for Calcium Oxalate Monohydrate Crystals

Crystal Retention in Renal Stone Disease

Contact Info

Product

Resources

About