Effects of Human Alpha-1-Acid Glycoprotein on Aminonucleoside- Induced Minimal Change Nephrosis in Rats

Muchitsch, Eva-Maria; Pichler, Ludwig; Schwarz, Hans; Walter, Ulrich

doi:10.1159/000045276

Cited by 14 publications

(9 citation statements)

References 11 publications

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“…Indeed, we have confirmed this composition in a previous report [8]by demonstrating reduced signal fluorescence in FITC-conjugated poly- L -lysine-stained sections of normal renal tissue following treatment with the enzymes neuraminidase, chondroitinase, heparitinase or hyaluronidase. Among these components, sialoglycoproteins in the glycocalyx of glomerular podocytes and fenestrated epithelium and heparan sulfate proteoglycan networks in the GBM have been attributed to be major constituents of this charge-selective barrier [22, 23]. Acidic methylation and its reversal by demethylation with brief saponification have become established as a means of differentiating sulfate and carboxyl staining [13], and we adopted this technique to distinguish heparan sulfate proteoglycan networks from sialoglycoproteins.…”

Section: Discussionmentioning

confidence: 99%

Analysis of Glomerular Anionic Charge Status in Children with IgA Nephropathy Using Confocal Laser Scanning Microscopy

Sakagami

Nakajima²,

Takagawa³

et al. 2004

Nephron Clin Pract

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Background: The proteinuria resulting from IgA nephropathy is secondary to altered charge-selective and/or size-selective properties of the glomerular capillary walls. However, the functional changes occurring within the glomerular capillary network which lead to proteinuria are still poorly understood. In this study, we analyzed the participation of charged components in the glomerular capillary and their role with respect to proteinuria in childhood IgA nephropathy. Methods: We examined glomerular anionic charge in renal biopsy specimens with confocal laser scanning microscopy using FITC-conjugated poly-L-lysine as a cationic tracer. The renal specimens investigated were from 9 children with IgA nephropathy (IgAN(+)) associated with detectable proteinuria in a morning urine specimen, 8 children with IgA nephropathy (IgAN(–)) and 11 children with thin basement membrane disease (TBMD) with no detectable proteinuria. Results: The labeling intensity of glomerular fixed anionic sites from IgAN(+) was significantly lower than that of IgAN(–) and TBMD. Staining the serial sections following methylation treatment revealed that the labeling intensity for fixed anionic sites in TBMD was significantly higher than that of both IgAN(+) and IgAN(–). On the other hand, saponification treatment resulted in significantly more intensive fluorescence in TBMD and IgAN(–) than in IgAN(+). Furthermore, statistical analysis demonstrated a significant correlation between 24-hour protein excretion and the intensity of fixed anionic sites in all patients with IgA nephropathy at pH 7.0 and following staining with saponification treatment. Conclusions: These findings suggest that a reduction of glomerular anionic charge might be causally associated with the development of proteinuria in childhood IgA nephropathy. Furthermore, sulfate components such as heparan sulfate proteoglycan might be involved initially followed by carboxyl components such as sialoglycoproteins in the glomeruli of patients with IgA nephropathy contributing to the occurrence of proteinuria. We suggest that this method represents a straightforward approach to dissect the participation of charged components in the pathogenesis of childhood IgA nephropathy and their relationship to the development of glomerular proteinuria.

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Section: Discussionmentioning

confidence: 99%

Analysis of Glomerular Anionic Charge Status in Children with IgA Nephropathy Using Confocal Laser Scanning Microscopy

Sakagami

Nakajima²,

Takagawa³

et al. 2004

Nephron Clin Pract

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“…A few years ago, it was suggested that orosomucoid may have therapeutic effects in certain nephrotic syndromes. Thus, intravenous injections of orosomucoid to rats with PAN nephrosis reduced the degree of proteinuria and improved podocyte morphology [12]. That study is the only report of an antiproteinuric effect of orosomucoid and it mainly focused on the morphological alterations.…”

Section: Introductionmentioning

confidence: 95%

Beneficial effects of orosomucoid on the glomerular barrier in puromycin aminonucleoside-induced nephrosis

Hjalmarsson¹,

Lidell²,

Haraldsson³

2006

Nephrology Dialysis Transplantation

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“…AGP also has renoprotective effects. It has been reported that exogenously administered AGP exerts protective effects against several types of renal damage including aminonucleoside-induced minimal change nephrosis 17 , puromycin-induced renal injury 18 and ischemia/reperfusion injury 19 . In our recent studies, we found that AGP is protective against obstructive nephropathy and renal fibrosis 20 .…”

mentioning

confidence: 99%

A synthetic retinoic acid receptor agonist Am80 ameliorates renal fibrosis via inducing the production of alpha-1-acid glycoprotein

Watanabe

Murata

et al. 2020

Sci Rep

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Renal fibrosis is a major factor in the progression of chronic kidney disease and the final common pathway of kidney injury. Therefore, the effective therapies against renal fibrosis are urgently needed. The objective of this study was to investigate the effect of Am80, a synthetic retinoic acid receptor (RAR) agonist, in the treatment of renal interstitial fibrosis using unilateral ureteral obstruction (UUO) mice. The findings indicate that Am80 treatment suppressed renal fibrosis and inflammation to the same degree as the naturally-occuring retinoic acid, all-trans retinoic acid (atRA). But the adverse effect of body weight loss in Am80-treated mice was lower compared to the atRA treatment. The hepatic mRNA levels of alpha-1-acid glycoprotein (AGP), a downstream molecule of RAR agonist, was increased following administration of Am80 to healthy mice. In addition, increased AGP mRNA expression was also observed in HepG2 cells and THP-1-derived macrophages that had been treated with Am80. AGP-knockout mice exacerbated renal fibrosis, inflammation and macrophage infiltration in UUO mice, indicating endogenous AGP played an anti-fibrotic and anti-inflammatory role during the development of renal fibrosis. We also found that no anti-fibrotic effect of Am80 was observed in UUO-treated AGP-knockout mice whereas atRA treatment tended to show a partial anti-fibrotic effect. These collective findings suggest that Am80 protects against renal fibrosis via being involved in AGP function. Approximately 10% of the world's population are affected by chronic kidney disease (CKD). CKD is associated with a risk of end-stage renal disease (ESRD), which is fatal without kidney replacement therapy such as dialysis or kidney transplantation 1,2. Renal fibrosis is the main factor in CKD progression and the final common pathway of kidney injury 3,4. Although initial fibrosis is thought to play a beneficial role in maintaining the kidney structure upon injury and repair 5 , the development of fibrosis causes a progressive decline in renal function 6. Therefore, effective therapies against renal fibrosis are urgently needed. It is known that retinoids, derivatives of vitamin A (retinol), regulate embryonic development and cellular differentiation 7. All-trans retinoic acid (atRA) is a natural retinoic acid that is clinically used for treating patients with acute promyelocytic leukemia. Retinoids are also of interest for their renoprotective and anti-inflammatory effects. In fact, atRA treatment was reported to suppress renal fibrosis in a unilateral ureteral obstruction

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Effects of Human Alpha-1-Acid Glycoprotein on Aminonucleoside- Induced Minimal Change Nephrosis in Rats

Cited by 14 publications

References 11 publications

Analysis of Glomerular Anionic Charge Status in Children with IgA Nephropathy Using Confocal Laser Scanning Microscopy

Analysis of Glomerular Anionic Charge Status in Children with IgA Nephropathy Using Confocal Laser Scanning Microscopy

Beneficial effects of orosomucoid on the glomerular barrier in puromycin aminonucleoside-induced nephrosis

A synthetic retinoic acid receptor agonist Am80 ameliorates renal fibrosis via inducing the production of alpha-1-acid glycoprotein

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