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  • 1
    Electronic Resource
    Electronic Resource
    Role of megalin, a proximal tubular endocytic receptor, in the pathogenesis of diabetic and metabolic syndrome-related nephropathies: protein metabolic overload hypothesis (2005)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 10 (2005), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: SUMMARY:  Megalin is an endocytic receptor on the apical membranes of proximal tubule cells (PTC) in the kidney, and is involved in the reabsorption and metabolism of various proteins that have been filtered by glomeruli. Patients with diabetes, especially type 2 diabetes, or metabolic syndrome are likely to have elevated serum levels of advanced glycation end products, liver-type fatty acid binding protein, angiotensin II, insulin and leptin, and renal metabolism of these proteins is potentially overloaded. Some of these proteins are themselves nephrotoxic, while others are carriers of nephrotoxic molecules. Megalin is involved in the proximal tubular uptake of these proteins. We hypothesize that megalin-mediated metabolic overload in PTC leads to compensatory cellular hypertrophy and sustained Na+ reabsorption, causing systemic hypertension and glomerular hyperfiltration via tubuloglomerular feedback, and named this as ‘protein metabolic overload hypothesis’. Impaired metabolism of bioactive proteins such as angiotensin II and insulin in PTC may enhance hypertrophy of PTC and/or Na+ reabsorption. Sleep apnoea syndrome, a frequent complication of diabetes and metabolic syndrome, may cause renal hypoxia and result in relative overload of protein metabolism in the kidneys. The development of strategies to identify patients with diabetes or metabolic syndrome who are at high risk for renal metabolic overload would allow intensive treatment of these patients in an effort to prevent the development of nephropathy. Further studies on the intracellular molecular signalling associated with megalin-mediated metabolic pathways may lead to the development of novel strategies for the treatment of nephropathies related to diabetes and metabolic syndrome.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.2005.00453.x
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  • 2
    Electronic Resource
    Electronic Resource
    No linkage to the COL4A3 gene locus in Japanese thin basement membrane disease families (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Nephrology 1 (1995), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Summary: Patients with thin basement membrane disease (TBMD) exhibit persistent haematuria with a diffuse thinning of the glomerular basement membrane (GBM), especially of the lamina densa. It appears to be an autosomal dominant trait. It has been reported that the Goodpasture epitope, which is located in the non-collagenous domain of type IV collagen α 3 chain, may be reduced in patients with TBMD. We speculated that the candidate gene for TBMD could be the type IV collagen α 3 chain gene (COL4A3), which is present closely to type IV collagen α 4 chain gene (COL4A4) on chromosome 2q35–37. We conducted a linkage analysis to investigate the relationship between familial TBMD and COL4A3 gene, using COL4A3 cDNA polymorphism and a (CA)n microsatellite marker located in the COL4A3 gene. We examined 32 individuals from four Japanese families with TBMD. There were no associations between the patients with haematuria and certain alleles of the two markers in the pedigrees of three families. It has been reported that type IV collagen α 1 chain gene (COL4A1) and α 2 chain gene (COL4A2) are not involved in TBMD, and that α 5 chain gene (COL4A5) and a 6 chain gene (COL4A6) map to chromosome X. In conclusion, our findings suggested that familial TBMD is not caused by the genetic abnormalities of type IV collagen genes isolated thus far.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1440-1797.1995.tb00046.x
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  • 3
    Electronic Resource
    Electronic Resource
    The prevention of glomerulosclerosis in rats using traditional Chinese medicine, Sairei-to (2000)
    Melbourne, Australia : Blackwell Science Pty
    Nephrology 5 (2000), S. 0 
    Details
    ISSN: 1440-1797
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: The effects of Sairei-to on chronic irreversible lesions were examined by the administration of drugs after the initiation of irreversible renal lesions by uninephrectomy and anti-thy-1 antibody injection. Twenty-one female Wistar rats were divided into three groups. Group 1 was treated with phosphate-buffered saline (PBS) as a control and groups 2 and 3 were treated with Sairei-to 400 mg/kg bodyweight per day on a daily basis beginning on day 1 (group 2) and day 7 (group 3) to day 42 after the intravenous administration of 500 μg anti-thy-1 monoclonal antibody (MoAb) into uninephrectomized rats, respectively. Statistically significant effects of Sairei-to on proteinuria were observed on days 3, 7, 14, and 21 in group 2 and on day 21 in group 3 as compared with the PBS controls. On day 42, light microscopy showed that Sairei-to ameliorated morphological lesions (Matrix score: 133.7 ± 50.35 for group 1 vs 40.0 ± 24.0 for group 2, P 〈 0.05). The weight of the kidneys in groups given Sairei-to was also lower than that in the PBS control. In addition, immunofluorescent findings showed that Sairei-to suppressed the expression of transforming growth factor-beta (TGF-β), alpha-smooth muscle actin (α-SMA) and collagen type I in glomeruli and decreased the number of ED1- and OX8-positive cells in tubulo-interstitium as well as in glomeruli. In conclusion, Sairei-to blocked the progression of renal lesions in this model even when it was administered after the initiation of the disease. In addition, earlier treatment more effectively prevented the progression of the renal lesions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1046/j.1440-1797.2000.00503.x
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  • 4
    Electronic Resource
    Electronic Resource
    Cloning and chromosomal mapping of a novel ABC transporter gene (hABC7), a candidate for X-linked sideroblastic anemia with spinocerebellar ataxia (1998)
    Springer
    Journal of human genetics 43 (1998), S. 115-122 
    Details
    ISSN: 1435-232X
    Keywords: Key words ABC transporter ; Mitochondria ; Heme ; Xq13 ; X-linked sideroblastic anemia with spinocerebellar ataxia
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Abstract We isolated a novel human ATP-binding cassette (ABC) transporter cDNA, determined its nucleotide sequence, and designated it human ABC7 (hABC7). The nucleotide sequence was highly homologous to the ATM1 gene in yeast, which encodes an ABC transporter (yAtm1p) located in the mitochondrial inner membrane. The deduced human product, a putative half-type transporter, consists of 752 amino acids that are 48.9% identical to those of yAtm1p. A computer-assisted protein structural and localization analysis revealed that the mitochondrial targeting signal of yAtm1p is conserved in the N-terminal region of the primary sequence of the hABC7 protein, and therefore this product is also likely to be located in the mitochondrial inner membrane. The evidence strongly suggests that the hABC7 gene is a counterpart of ATM1 and that its product is probably involved in heme transport. We mapped the hABC7 gene to chromosome Xq13.1–q13.3 by fluorescence in-situ hybridization. As band Xq13 has been implicated in X-linked sideroblastic anemia with spinocerebellar ataxia, hABC7 becomes a candidate gene for this heritable disorder.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s100380050051
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    Paper (German National Licenses)
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