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  • 1
    Online Resource
    Online Resource
    Induction of albuminuria and kidney damage in SHR by transfer of chromosome 8 from Munich Wistar Frömter rats
    American Physiological Society ; 2012
    In:  Physiological Genomics Vol. 44, No. 1 ( 2012-01), p. 110-116
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 44, No. 1 ( 2012-01), p. 110-116
    Abstract: Inbred Munich Wistar Frömter [MWF/FubRkb (RGD:724569), MWF] rats develop progressive albuminuria with age that is under polygenetic influence. We previously identified a major albuminuria quantitative trait locus (QTL) on rat chromosome (RNO)8 in MWF. To test the independent role of QTL(s) for albuminuria development on RNO8, we generated a consomic SHR-Chr 8 MWF /Rkb (SHR-8 MWF ) strain by transferring RNO8 from MWF into the albuminuria-resistant background of the spontaneously hypertensive rat [SHR/FubRkb (RGD:631696; SHR)]. Young male MWF, SHR, and SHR-8 MWF were sham-operated or unilaterally nephrectomized (Nx) at 6 wk and followed up to 24 wk of age, respectively. Systolic blood pressure was significantly lower in SHR-8 MWF Sham compared with SHR Sham (−19.4 mmHg, P = 0.03) at 24 wk. In contrast, transfer of MWF-RNO8 into SHR induced a significant elevation of urinary albumin excretion (UAE) between weeks 12 and 24 in SHR-8 MWF compared with SHR Sham animals ( P 〈 0.0001, respectively). Nx resulted in a significant increase in UAE in both strains during follow-up ( P 〈 0.0001, respectively), with significant higher values in SHR-8 MWF compared with SHR ( P 〈 0.005, respectively). Renal structural changes as determined by glomerulosclerosis (GSI) and tubulointerstitial damage index (TDI) were significantly higher in consomic animals either at Sham (TDI) or Nx (GSI) conditions ( P 〈 0.05, respectively). These data confirm the independent role of MWF QTL(s) on RNO8 for both albuminuria and structural kidney damage. Moreover, this study shows for the first time the induction of albuminuria by transferring one or more albuminuria QTL into a resistant recipient background in a consomic rat strain.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00123.2011
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2012
    detail.hit.zdb_id: 2031330-5
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  • 2
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    Genetic locus on MWF rat chromosome 6 affects kidney damage in response to l -NAME treatment in spontaneously hypertensive rats
    American Physiological Society ; 2010
    In:  Physiological Genomics Vol. 42, No. 1 ( 2010-06), p. 126-133
    Details
    In: Physiological Genomics, American Physiological Society, Vol. 42, No. 1 ( 2010-06), p. 126-133
    Abstract: A major quantitative trait locus (QTL) on rat chromosome (RNO)6 was linked to albuminuria in Munich Wistar Frömter rats (MWF). We tested whether transfer of MWF RNO6 into the background of albuminuria-resistant spontaneously hypertensive rats (SHR) induces albuminuria in consomic SHR-6 MWF animals. Male MWF, SHR, and SHR-6 MWF were sham operated and treated between 6 and 24 wk of age with normal water (Sham) or with water containing 20 mg/l N G -nitro-l-arginine methyl ester (l-NAME) or unilaterally nephrectomized (Nx). Compared with SHR albuminuria was not increased in SHR-6 MWF in both Sham and Nx groups. All animals survived the observation period in Sham and Nx groups, while premature mortality occurred from 12–14 wk on in l-NAME-treated SHR and SHR-6 MWF compared with MWF l-NAME animals, in which survival was not affected ( P 〈 0.005, respectively). Subsequent further analysis of l-NAME-treated animals at 12 wk of age showed significantly increased arterial blood pressures in both SHR and SHR-6 MWF compared with control ( P 〈 0.05), with higher levels in SHR compared with consomics ( P 〈 0.05). However, l-NAME-treated consomic animals demonstrated increased albuminuria compared with SHR (12.7 ± 3.5 vs. 0.8 ± 0.2 mg/24 h; P 〈 0.05) and an induction of tubulointerstitial structural injury and expression of neutrophil gelatinase-associated lipocalin mRNA ( P 〈 0.05 vs. other strains). Our study demonstrates that isolation of the RNO6 albuminuria QTL from the MWF background and transfer into SHR fails to induce an albuminuria phenotype during normal conditions or after nephron reduction. Moreover, our data indicate that genes on RNO6 contribute to the development of l-NAME-induced renal damage in the SHR strain.
    Type of Medium: Online Resource
    ISSN: 1094-8341 , 1531-2267
    URL: Article
    DOI: 10.1152/physiolgenomics.00036.2010
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2010
    detail.hit.zdb_id: 2031330-5
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  • 3
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    Genetic Variants on Rat Chromosome 8 Exhibit Profound Effects on Hypertension Severity and Survival During Nitric Oxide Inhibition in Spontaneously Hypertensive Rats
    Oxford University Press (OUP) ; 2014
    In:  American Journal of Hypertension Vol. 27, No. 3 ( 2014-3), p. 294-298
    Details
    In: American Journal of Hypertension, Oxford University Press (OUP), Vol. 27, No. 3 ( 2014-3), p. 294-298
    Type of Medium: Online Resource
    ISSN: 1941-7225 , 0895-7061
    URL: Article
    DOI: 10.1093/ajh/hpt236
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2014
    detail.hit.zdb_id: 1479505-X
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  • 4
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    Elimination of Severe Albuminuria in Aging Hypertensive Rats by Exchange of 2 Chromosomes in Double-Consomic Rats
    Ovid Technologies (Wolters Kluwer Health) ; 2011
    In:  Hypertension Vol. 58, No. 2 ( 2011-08), p. 219-224
    Details
    In: Hypertension, Ovid Technologies (Wolters Kluwer Health), Vol. 58, No. 2 ( 2011-08), p. 219-224
    Abstract: The inherited nephron deficit and progressive albuminuria development observed in hypertensive Munich Wistar Frömter (MWF) rats are influenced by quantitative trait loci on rat chromosome (RNO) 6 and RNO8. Previous studies in young MWF rats suggested that the nephron deficit represents a cause for glomerular hypertrophy preceding onset of albuminuria at 8 weeks and demonstrated a simultaneous induction of the podocyte stress marker desmin and podoplanin loss in podocytes. Here we investigated the separate genetic influence of RNO6 and RNO8 on early glomerular changes and subsequent albuminuria in single-consomic MWF rats in which RNO6 (MWF-6 SHR ) and RNO8 (MWF-8 SHR ) were replaced by the respective spontaneously hypertensive rat (SHR) chromosome. Furthermore, we tested the role of synergistic effects between both chromosomes in a double-consomic MWF-6 SHR 8 SHR strain. Increased glomerular, extramesangial desmin expressions at 6 and albuminuria at 8 weeks were significantly reduced in single- and double-consomics ( P 〈 0.05 versus MWF, respectively). MWF-6 SHR 8 SHR rats demonstrated the lowest desmin expression and glomerular volume ( P 〈 0.05 versus MWF, MWF-6 SHR , and MWF-8 SHR , respectively), indicating synergistic effects between RNO6 and RNO8. A significant and similar loss of podoplanin was only seen in MWF and MWF-6 SHR rats but not in MWF-8 SHR and MWF-6 SHR 8 SHR rats ( P 〈 0.02, respectively); this refutes a mandatory coupling of desmin induction and podoplanin loss in podocytes preceding albuminuria and reveals a genetic link between RNO8 and loss of podoplanin protein. Long-term follow up in MWF-6 SHR 8 SHR rats demonstrates the relevance of the absence of glomerular changes in young animals, because double-consomics demonstrate a complete suppression of progressive albuminuria and kidney damage compared with MWF rats despite similar blood pressures.
    Type of Medium: Online Resource
    ISSN: 0194-911X , 1524-4563
    URL: Article
    DOI: 10.1161/HYPERTENSIONAHA.111.170621
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2011
    detail.hit.zdb_id: 2094210-2
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