Inhibitory effect of calcium phosphate‐associated proteins on calcium oxalate crystallization: α2‐HS‐glycoprotein, prothrombin‐F1 and osteopontin

Nishio, Shunji; Iseda, Tokuhiro; Takeda, Hisashi; Iwata, Hidenobu; Yokoyama, Masaru

doi:10.1046/j.1464-410x.2000.00791.x

Cited by 11 publications

(10 citation statements)

References 31 publications

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“…Clinical studies to date are inconclusive regarding the relationship between OPN and renal stone disease. Some investigators have reported decreased concentrations of OPN in urine from stone formers compared to normal individuals [123], while others have not [167]. A single-base mutation in the OPN gene is seen at significantly higher incidence in patients with recurrent stone formation or familial nephrolithiasis [168].…”

Section: Matrix Componentsmentioning

confidence: 99%

Nephrolithiasis: Molecular Mechanism of Renal Stone Formation and the Critical Role Played by Modulators

Aggarwal

Narula

Kakkar³

et al. 2013

BioMed Research International

257

232

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Urinary stone disease is an ailment that has afflicted human kind for many centuries. Nephrolithiasis is a significant clinical problem in everyday practice with a subsequent burden for the health system. Nephrolithiasis remains a chronic disease and our fundamental understanding of the pathogenesis of stones as well as their prevention and cure still remains rudimentary. Regardless of the fact that supersaturation of stone-forming salts in urine is essential, abundance of these salts by itself will not always result in stone formation. The pathogenesis of calcium oxalate stone formation is a multistep process and essentially includes nucleation, crystal growth, crystal aggregation, and crystal retention. Various substances in the body have an effect on one or more of the above stone-forming processes, thereby influencing a person's ability to promote or prevent stone formation. Promoters facilitate the stone formation while inhibitors prevent it. Besides low urine volume and low urine pH, high calcium, sodium, oxalate and urate are also known to promote calcium oxalate stone formation. Many inorganic (citrate, magnesium) and organic substances (nephrocalcin, urinary prothrombin fragment-1, osteopontin) are known to inhibit stone formation. This review presents a comprehensive account of the mechanism of renal stone formation and the role of inhibitors/promoters in calcium oxalate crystallisation.

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Section: Matrix Componentsmentioning

confidence: 99%

Nephrolithiasis: Molecular Mechanism of Renal Stone Formation and the Critical Role Played by Modulators

Aggarwal

Narula

Kakkar³

et al. 2013

BioMed Research International

257

232

View full text Add to dashboard Cite

show abstract

“…OPN is synthesized within the kidney and is present in human urine at levels that can effectively inhibit CaOx crystallization [21][22][23]. Indeed, reduced concentrations of OPN have been documented in urine from patients with renal stone disease compared with normal individuals [24,25]. In vitro data indicate that urinary OPN may inhibit the nucleation, growth, and aggregation of CaOx crystals in cultured renal epithelial cells [26][27][28].…”

Section: Introductionmentioning

confidence: 99%

Role of osteopontin in early phase of renal crystal formation: immunohistochemical and microstructural comparisons with osteopontin knock-out mice

et al. 2011

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Osteopontin (OPN) is an important matrix protein of renal calcium stone. However, the function of OPN in the early phase of renal crystal formation is not well defined. In this study, we examined OPN expression in the early phase of renal crystal formation with ultra-microstructural observations and immuno-TEM (transmission electron microscopy) in control and OPN knock-out (OPN-KO) mice. Glyoxylate (100 mg/kg) was intra-abdominally administered to male wild-type mice (C57BL/6, 8 weeks of age) and OPN-KO mice (C57BL/6, 8 weeks of age). Kidney was collected before and 6, 12, and 24 h after administration. We examined the relation between renal crystal formation and microstructural OPN location using TEM and immunohistochemical staining of OPN as well as western blotting and quantitative RT-PCR for OPN. OPN protein expression gradually increased in the renal cortex-medulla junction after glyoxylate administration, and OPN mRNA was increased until 12 h, but decreased at 24 h. In ultra-microstructural observation, OPN began to appear on the luminal side of renal distal tubular cells at 6 h and was gradually detected in the tubular lumen at 12 h. OPN was present in the crystal nuclei and collapsed mitochondria in the tubular lumen. In the OPN-KO mice, collapsed mitochondria were present, but no crystal nuclei formation were detected at 24 h. Based on the results this study proposed that the appearance of organelles, such as mitochondria and microvilli, in the tubular lumen after cell injury may be the starting point of crystal nucleus formation due to the aggregation ability of OPN.

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“…Genetic factors that regulate calcium metabolism and inflammation are possibly linked with nephrolithiasis. Genetic polymorphisms of CLDN14, CASR, OPN, ORAI1, and VDR were reported to be involved in calcium nephrolithiasis in humans [19–23]. Our previous study indicated that genetic polymorphisms of ORAI1 are associated with susceptibility to calcium urolithiasis [6].…”

Section: Discussionmentioning

confidence: 99%

Study of the Association betweenITPKCGenetic Polymorphisms and Calcium Nephrolithiasis

Kan

Chou

Chiu

et al. 2014

BioMed Research International

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Nephrolithiasis is a multifactorial disease caused by environmental, hormonal, and genetic factors. Genetic polymorphisms of ORAI1, which codes for the main subunit of the store-operated calcium (SOC) channel, were reported to be associated with the risk and recurrence of calcium nephrolithiasis. Inositol 1,4,5-trisphosphate (IP3) 3-kinase C (ITPKC) is a negative regulator of the SOC channel-mediated signaling pathway. We investigated the association between calcium containing nephrolithiasis and genetic variants of ITPKC gene in Taiwanese patients. 365 patients were recruited in this study. Eight tagging single nucleotide polymorphisms of ITPKC were selected for genotyping. ITPKC genotypes were determined by TaqMan assay. ITPKC plasmids were transfected into cells to evaluate the intracellular calcium mobilization. Our results indicated that rs2607420 CC genotype in the intron region of the ITPKC gene is associated with a lower eGFR by both Modification of Diet in Renal Diseases (P = 0.0405) and Cockcroft-Gault (P = 0.0215) equations in patients with calcium nephrolithiasis. Our results identify a novel polymorphism for renal function and highlight the importance of ITPKC as a key molecule to regulate calcium signaling.

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Inhibitory effect of calcium phosphate‐associated proteins on calcium oxalate crystallization: α2‐HS‐glycoprotein, prothrombin‐F1 and osteopontin

Cited by 11 publications

References 31 publications

Nephrolithiasis: Molecular Mechanism of Renal Stone Formation and the Critical Role Played by Modulators

Nephrolithiasis: Molecular Mechanism of Renal Stone Formation and the Critical Role Played by Modulators

Role of osteopontin in early phase of renal crystal formation: immunohistochemical and microstructural comparisons with osteopontin knock-out mice

Study of the Association betweenITPKCGenetic Polymorphisms and Calcium Nephrolithiasis

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