Mechanisms involved in calcium oxalate endocytosis by Madin-Darby canine kidney cells

Campos, Alexandre; Schor, Nestor

doi:10.1590/s0100-879x2000000100015

Cited by 14 publications

(9 citation statements)

References 26 publications

(21 reference statements)

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“…In addition endocytosis is inhibited by an increase in intracellular calcium. There is generalized reorganization of intermediate filaments and concentration of F actin at the sites of internalized crystals [15]. Furthermore prevention of cytoskeleton assembly by cytochalasin B and colchicine inhibits CaOx crystal internalization by MDCK cells.…”

Section: Crystal Endocytosis and Cell Proliferationmentioning

confidence: 99%

Role of Renal Epithelial Cells in the Initiation of Calcium Oxalate Stones

Khan¹

2004

Nephron Exp Nephrol

111

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Normal urinary environment is inhibitory to crystallization. Occasional crystals are internalized by the renal epithelial cells and sequestered to lysosomes or externalized into the interstitium to be handled by the inflammatory cells. Elevated levels of oxalate and calcium oxalate crystals, however, provoke renal cells to increase the synthesis of osteopontin, bikunin, heparan sulfate proteoglycan, monocyte chemoattractant protein-1, and prostaglandin E₂, which are known mediators of the inflammatory processes and extracellular matrix production. Osteopontin and bikunin are also modulators of crystallization. Exposed renal epithelial cells are often injured and go through apoptosis and/or necrosis initiating a cascade of events leading to further crystallization, crystal retention and development of stone nidi. Reactive oxygen species are produced during the interactions between the oxalate/crystals and renal cells and are responsible for the various cellular responses. Calcium oxalate crystal deposition in the rat kidneys also activates the renin-angiotensin system. Both oxalate and calcium oxalate crystals selectively activate p38 mitogen-activated protein kinase in the exposed tubular cells. Extracellular environment changes from one that inhibits crystal nucleation, growth, aggregation and retention to that, which promotes these processes.

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Section: Crystal Endocytosis and Cell Proliferationmentioning

confidence: 99%

Role of Renal Epithelial Cells in the Initiation of Calcium Oxalate Stones

Khan¹

2004

Nephron Exp Nephrol

111

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“…This mechanism would lead to fewer stones, lesser calculus formation, and thus, amelioration of the symptoms. Thus, besides having a role in protein endocytosis, the ClC-5 channel may also be responsible for the clearance of the calculi formed within the kidney tubules since both protein and calculi are endocytosed by similar mechanisms (29,38,39). Taken together, the data addressing the role of ClC-5 in protein endocytosis indicate that ClC-5 may also be important for calculus clearance.…”

Section: Clc-5 Chloride Channel and Protein Endocytosismentioning

confidence: 91%

“…Several investigators have postulated that in the renal tubule the calculi are cleared by endocytosis (8,9,38,39). This mechanism would lead to fewer stones, lesser calculus formation, and thus, amelioration of the symptoms.…”

Section: Clc-5 Chloride Channel and Protein Endocytosismentioning

confidence: 99%

ClC-5 chloride channel and kidney stones: what is the link?

Silva

Morales

Lopes

2001

Braz J Med Biol Res

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Nephrolithiasis is one of the most common diseases in the Western world. The disease manifests itself with intensive pain, sporadic infections, and, sometimes, renal failure. The symptoms are due to the appearance of urinary stones (calculi) which are formed mainly by calcium salts. These calcium salts precipitate in the renal papillae and/ or within the collecting ducts. Inherited forms of nephrolithiasis related to chromosome X (X-linked hypercalciuric nephrolithiasis or XLN) have been recently described. Hypercalciuria, nephrocalcinosis, and male predominance are the major characteristics of these diseases. The gene responsible for the XLN forms of kidney stones was cloned and characterized as a chloride channel called ClC-5. The ClC-5 chloride channel belongs to a superfamily of voltage-gated chloride channels, whose physiological roles are not completely understood. The objective of the present review is to identify recent advances in the molecular pathology of nephrolithiasis, with emphasis on XLN. We also try to establish a link between a chloride channel like ClC-5, hypercalciuria, failure in urine acidification and protein endocytosis, which could explain the symptoms exhibited by XLN patients.

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“…52 CaOx endocytosis experiments Calcium oxalate endocytosis was determined using flow cytometry at 488 nm excitation as previously described. 53 In brief, the flow cytometer detects how cells scatter the incident light from a focused laser beam and emit fluorescence. In forward-scatter, the light is diffracted at low angles, generally proportional to cell size.…”

Section: Lactate Dehydrogenase Assaymentioning

confidence: 99%

Mouse interleukin-20 receptor 1a targets renal epithelial cells and is associated with renal calcium deposition

Wei

Chang

2008

Genes Immun

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We previously identified a novel transcript, mouse (m)IL-20R1a, generated by alternative splicing of the mIL-20R1 gene and studied its possible in vitro functions. However, the function of mIL-20R1a in vivo is unknown. Overexpression of mIL-20R1a in transgenic FvB/N mice resulted in the pathological change of excess calcium deposited in the kidneys. The interplay between renal epithelial cells and calcium oxalate (CaOx) was important in the crystallization involved in the formation of renal stones (nephrolithiasis). Thus, we investigated and compared the responses of mouse renal proximal (TKPTS) and collecting (M-1) tubule cell lines to CaOx with or without mIL-20R1a. The renal epithelial cell lines exposed to CaOx in the presence of mIL20R1a showed significantly increased lactate dehydrogenase release; loss of cell viability through apoptosis; increased CaOx internalization; higher tumor necrosis factor (TNF)-a, MCP-1 and RANTES expression; and higher reactive oxygen species production. Interleukin-6, TNF-a and MCP-1 were also upregulated in the kidneys of mIL-20R1a transgenic mice. These effects of mIL-20R1a on CaOx-exposed renal epithelial cells showed that mIL-20R1a functioned as an aggravating factor in promoting calcium deposition in kidney of mice.

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Mechanisms involved in calcium oxalate endocytosis by Madin-Darby canine kidney cells

Cited by 14 publications

References 26 publications

Role of Renal Epithelial Cells in the Initiation of Calcium Oxalate Stones

Role of Renal Epithelial Cells in the Initiation of Calcium Oxalate Stones

ClC-5 chloride channel and kidney stones: what is the link?

Mouse interleukin-20 receptor 1a targets renal epithelial cells and is associated with renal calcium deposition

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