Osteopontin and Tamma-Horsefall proteins – Macromolecules of myriad values

Mohamaden, Walaa I.; Wang, Heng; Guan, Huawei; Meng, Xianli; Li, Jianji

doi:10.1016/j.jobaz.2014.03.002

Cited by 10 publications

(7 citation statements)

References 42 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In addition to exaggerated oxidative stress, the present study demonstrated loss of anticrystallization defenses, such as hypocitraturia, hypomagnesuria, and low renal OPN and THP expression, in HP kidneys (Figs 2 and 9 ). These results are consistent with those of previous reports [ 12 , 19 , 30 ] and clearly indicate deficient defense against CaOx formation in the hyperoxaluric kidney. Hypocitraturia and loss of THP and OPN were worse in HS+HP kidneys, especially at 42 days of treatment, than in HP kidneys (Figs 2 and 9 ).…”

Section: Discussionsupporting

confidence: 94%

See 1 more Smart Citation

High Sodium-Induced Oxidative Stress and Poor Anticrystallization Defense Aggravate Calcium Oxalate Crystal Formation in Rat Hyperoxaluric Kidneys

Huang

Chieh

2015

PLoS ONE

View full text Add to dashboard Cite

Enhanced sodium excretion is associated with intrarenal oxidative stress. The present study evaluated whether oxidative stress caused by high sodium (HS) may be involved in calcium oxalate crystal formation. Male rats were fed a sodium-depleted diet. Normal-sodium and HS diets were achieved by providing drinking water containing 0.3% and 3% NaCl, respectively. Rats were fed a sodium-depleted diet with 5% hydroxyl-L-proline (HP) for 7 and 42 days to induce hyperoxaluria and/or calcium oxalate deposition. Compared to normal sodium, HS slightly increased calcium excretion despite diuresis; however, the result did not reach statistical significance. HS did not affect the hyperoxaluria, hypocalciuria or supersaturation caused by HP; however, it increased calcium oxalate crystal deposition soon after 7 days of co-treatment. Massive calcium oxalate formation and calcium crystal excretion in HS+HP rats were seen after 42 days of treatment. HP-mediated hypocitraturia was further exacerbated by HS. Moreover, HS aggravated HP-induced renal injury and tubular damage via increased apoptosis and oxidative stress. Increased urinary malondialdehyde excretion, in situ superoxide production, NAD(P)H oxidase and xanthine oxidase expression and activity, and decreased antioxidant enzyme expression or activity in the HS+HP kidney indicated exaggerated oxidative stress. Interestingly, this redox imbalance was associated with reduced renal osteopontin and Tamm-Horsfall protein expression (via increased excretion) and sodium-dependent dicarboxylate cotransporter NaDC-1 upregulation. Collectively, our results demonstrate that a HS diet induces massive crystal formation in the hyperoxaluric kidney; this is not due to increased urinary calcium excretion but is related to oxidative injury and loss of anticrystallization defense.

show abstract

Section: Discussionsupporting

confidence: 94%

“…OPN and THP are two important factors in the kidney that not only prevent CaOx crystal formation but also provide renoprotection [ 30 ]. After treatment with phenylephrine, rats fed a HS diet show hypertension associated with de novo synthesis of OPN in the kidneys [ 33 ].…”

Section: Discussionmentioning

confidence: 99%

High Sodium-Induced Oxidative Stress and Poor Anticrystallization Defense Aggravate Calcium Oxalate Crystal Formation in Rat Hyperoxaluric Kidneys

Huang

Chieh

2015

PLoS ONE

View full text Add to dashboard Cite

show abstract

“…The increase in OPN in rats with kidney stones induced by hyperoxaluria can be explained by 2 mechanisms, the first that the interaction between crystals and the membrane stimulates the production of OPN mRNA and protein which in turn triggers the adhesion of crystals to the renal epithelium and facilitates crystal aggregation causing blockade from the tubular lumen. This theory supports the role of OPN as a promoter of stone formation (29). Reports from previous studies found that hyperoxaluria and calcium oxalate crystal deposition in mice generally upregulate OPN expression (30).…”

Section: Kidney Stone Formationsupporting

confidence: 83%

The Role of Testosterone Hormone on Crystal Formation Through the Renal Expression of Osteopontin in Male Wistar Rat

2022

View full text Add to dashboard Cite

This study aims to investigate the role of testosterone hormone on crystal formation through osteopontin expression. This was an experimental study with post-test only control design. A total of 12 rats aged 10 weeks were divided into two groups which are male rats group fed with water containing EG (Ethylene Glycol) 0.75% and male rats group fed with water containing EG (Ethylene Glycol) 0.75% and were injected with testosterone hormone. Furthermore, the rats were observed and fed with standard diet for 30 days. Then, both groups were terminated. The kidneys were extracted and examined for Osteopontin expression. Histopathology examination was also performed in both groups The result of the study showed that the mean kidney osteopontin expression in male rats fed with water containing EG 0.75% and received testosterone hormone injection were significantly higher (29.16 ± 9.072) compared to male rat groups fed with water containing EG 0.75% alone (11.42 ± 3.692) with p value 0.001. Histopathology examination with HE stain revealed that both groups demonstrated the presence of stone in kidney tubules, kidney swelling and pelvic ectasis. This feature suggested the presentation of hydronephrosis as a result of stone obstruction. As a conclusion, this study shed light on the role of hormonal sex of testosterone involving in crystal formation through osteopontin expression. Keywords: urolithiasis, testosterone, sex hormone, osteopontin

show abstract

“…Consistant with the above-mentioned OPN structure, the protein is regarded to inhibit formation of both calcium oxalate and calcium phosphate crystals using the polyAsp sequence, thereby diminishing the concentration of mineral compounds in urine [42,43]. In that light, similarly to the Tamm-Horsfall protein (uromodulin), OPN may be a potent inhibitor of crystallization and a preventive factor of nucleation, growth, and aggregation of most common crystals found in urine and in kidney stones [44].…”

Section: Osteopontin and Inflammationmentioning

confidence: 99%

Physiological and pathophysiological implications of osteopontin and the diagnostic utility of the protein in kidney diseases

Dobrek¹

2018

J Pre Clin Clin Res.

View full text Add to dashboard Cite

Introduction and objective. Osteopontin (OPN) is a protein playing many pleiotropic both physiological and pathophysiological roles in various organs. The paper briefly characterizes both the positive and negative roles of OPN, with particular emphasis on the role of the protein in kidney functioning. Brief description of the state of knowledge. As its name suggests, OPN is a protein mainly regulating bone homeostasis, but it also participates in the pathogenesis of inflammation, neoplasm, atherosclerosis and vascular calcification. OPN is also an important protein involved in kidney physiology. Its main physiological function is to act as an inhibitor of the crystallization of urine mineral components and to prevent kidney stones formation. OPN is also overproduced in various kidney pathologies (tubulointerstitial fibrosis, crescending glomerulonephritis, cyclosporine or diabetic nephropathy, renal ischemia reperfusion injury), and both experimental and clinical studies suggest that OPN may exert either a protective or detrimental effect on kidneys. Conclusions. Considering the OPN role in kidneys, the protein is currently proposed as one of novel laboratory biomarkers for renal function. OPN, along with the other proteins found in the urine in various kidney diseases (neutrophil gelatinaseassociated lipocalin-1, kidney injury molecule-1, and fatty acid binding protein) is a part of the laboratory panel that will be gradually introduced into common laboratory practice.

show abstract

Osteopontin and Tamma-Horsefall proteins – Macromolecules of myriad values

Cited by 10 publications

References 42 publications

High Sodium-Induced Oxidative Stress and Poor Anticrystallization Defense Aggravate Calcium Oxalate Crystal Formation in Rat Hyperoxaluric Kidneys

High Sodium-Induced Oxidative Stress and Poor Anticrystallization Defense Aggravate Calcium Oxalate Crystal Formation in Rat Hyperoxaluric Kidneys

The Role of Testosterone Hormone on Crystal Formation Through the Renal Expression of Osteopontin in Male Wistar Rat

Physiological and pathophysiological implications of osteopontin and the diagnostic utility of the protein in kidney diseases

Contact Info

Product

Resources

About