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  • 1
    Online Resource
    Online Resource
    Pentoxifylline Inhibits Transforming Growth Factor-Beta Signaling and Renal Fibrosis in Experimental Crescentic Glomerulonephritis in Rats
    S. Karger AG ; 2009
    In:  American Journal of Nephrology Vol. 29, No. 1 ( 2009), p. 43-53
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 29, No. 1 ( 2009), p. 43-53
    Abstract: 〈 i 〉 Background/Aims: 〈 /i 〉 Pentoxifylline (PTX) has been shown to inhibit renal inflammation in a rat model of crescentic glomerulonephritis. The present study investigated the role of PTX in renal fibrosis in rats with crescentic glomerulonephritis. 〈 i 〉 Methods: 〈 /i 〉 A rat model of accelerated anti-glomerular basement membrane glomerulonephritis was induced and treated with PTX or vehicle control for 3, 7, 14 and 28 days. The therapeutic effect and mechanism of PTX on renal fibrosis were examined by Northern blot and immunohistochemistry. 〈 i 〉 Results: 〈 /i 〉 Diseased rats treated with vehicle control developed a severe crescentic glomerulonephritis with progressive renal fibrosis identified by a marked accumulation of α-SMA+ myofibroblasts and collagen matrix. This was associated with tubular epithelial-myofibroblast transition as evident by de novo expression of α-SMA and a loss of E-cadherin on damaged tubular epithelial cells. Further studies revealed that severe renal fibrosis was associated with upregulation of renal TGF-β1 and activation of TGF-β/Smad signaling, which was blocked by treatment with PTX. 〈 i 〉 Conclusions: 〈 /i 〉 PTX may be an anti-fibrosis agent capable of inhibiting renal fibrosis in a rat model of crescentic glomerulonephritis. Blockade of TGF-β1 expression and Smad2/3 activation may be a mechanism by which PTX inhibits renal fibrosis.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000150600
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2009
    detail.hit.zdb_id: 1468523-1
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  • 2
    Online Resource
    Online Resource
    Role of JAK/STAT Pathway in IL-6-Induced Activation of Vascular Smooth Muscle Cells
    S. Karger AG ; 2004
    In:  American Journal of Nephrology Vol. 24, No. 4 ( 2004), p. 387-392
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 24, No. 4 ( 2004), p. 387-392
    Abstract: 〈 i 〉 Background/Aims: 〈 /i 〉 IL-6, an inducer of the acute-phase response, is linked with the development of vascular disease and atherosclerosis. One mechanism likely involves direct effects of IL-6 on vascular smooth muscle cells (VSMC), for IL-6 can induce VSMC proliferation and the release of monocyte chemoattractant protein-1 (MCP-1). We hypothesized that this stimulation occurs via the JAK (janus-activated kinase)/STAT (signal and transducers and activators of transcription) signaling pathway. 〈 i 〉 Methods: 〈 /i 〉 Rat VSMC were stimulated with IL-6 in the presence or absence of a JAK 2 inhibitor, and the activation of STAT 3 (by Western), MCP-1 (by ELISA) and DNA synthesis (by 〈 sup 〉 3 〈 /sup 〉 H-thymidine incorporation) was determined. 〈 i 〉 Results: 〈 /i 〉 IL-6 rapidly induced phosphorylation of STAT 3 in a dose- and time-dependent manner with a peak expression at 30 min. IL-6 also stimulated MCP-1 protein production and DNA synthesis dose dependently. 50 µ 〈 i 〉 M 〈 /i 〉 of AG490, a specific JAK 2 inhibitor, partially inhibited STAT 3 activation and MCP-1 production, with near complete inhibition of DNA synthesis. 〈 i 〉 Conclusion: 〈 /i 〉 The JAK/STAT pathway partially mediates IL-6-induced MCP-1 production and DNA synthesis in rat VSMC. These studies implicate a role of the JAK/STAT pathway in the development of vascular disease and atherosclerosis.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000079706
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2004
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  • 3
    Online Resource
    Online Resource
    Amelioration of Albuminuria in ROCK1 Knockout Mice with Streptozotocin-Induced Diabetic Kidney Disease
    S. Karger AG ; 2011
    In:  American Journal of Nephrology Vol. 34, No. 5 ( 2011), p. 468-475
    Details
    In: American Journal of Nephrology, S. Karger AG, Vol. 34, No. 5 ( 2011), p. 468-475
    Abstract: 〈 i 〉 Background: 〈 /i 〉 Although blockade of Rho kinase with pharmacologic inhibitors ameliorates renal fibrosis and diabetic kidney disease (DKD), the underlined mechanisms remain largely unclear. The present study tested the hypothesis that ROCK1 may regulate the early development of albuminuria via the megalin/cubilin-dependent mechanism. 〈 i 〉 Methods: 〈 /i 〉 A DKD model was induced in ROCK1 knockout and wild-type mice by streptozotocin (STZ). The effect of deleted ROCK1 on urinary albumin excretion and the expression of megalin/cubilin were examined. In addition, the effect of blocking ROCK activities with an inhibitor (Y-27632) on tubular albumin reabsorption was tested in a normal rat tubular epithelial cell line (NRK52E) under high-glucose conditions. Expression of transforming growth factor (TGF)-β1, interleukin-1β and collagen-1 was also been examined. 〈 i 〉 Results: 〈 /i 〉 Urinary albumin excretion was significantly increased in ROCK1 WT mice at 8 weeks after STZ injection. In contrast, mice lacking ROCK1 gene were protected against the development of albuminuria. This was associated with the protection against the loss of megalin/cubilin and an increase in TGF-β 〈 sub 〉 1 〈 /sub 〉 , IL-1β, and fibrosis in the kidney. In vitro, we also found that blockade of Rho kinase with inhibitor Y-27632 prevented high-glucose-induced loss of megalin expression and an increase of TGF-β 〈 sub 〉 1 〈 /sub 〉 , thereby increasing the absorption rate of FITC-labeled albumin by tubular epithelial cells. 〈 i 〉 Conclusion: 〈 /i 〉 ROCK1 may play a role in the development of albuminuria in DKD by downregulating the endocytosis receptors complex – megalin/cubilin.
    Type of Medium: Online Resource
    ISSN: 0250-8095 , 1421-9670
    URL: Article
    DOI: 10.1159/000332040
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2011
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  • 4
    Online Resource
    Online Resource
    Role of Macrophage Migration Inhibition Factor in Kidney Disease
    S. Karger AG ; 2008
    In:  Nephron Experimental Nephrology Vol. 109, No. 3 ( 2008-7-25), p. e79-e83
    Details
    In: Nephron Experimental Nephrology, S. Karger AG, Vol. 109, No. 3 ( 2008-7-25), p. e79-e83
    Abstract: Macrophage migration inhibitory factor (MIF) has been shown to play a pathogenic role in kidney disease. This article will review the current understanding of the expression of MIF and its functional role in immune-mediated renal injury in both human and animal models of kidney disease. Upregulation of MIF is found in both human and experimental kidney disease including renal allograft rejection and contributes significantly to macrophage and T-cell accumulation and progressive renal injury. It is now clear that MIF is a stress factor, a pro-inflammatory cytokine, a growth factor and a hormone. MIF acts through many mechanisms to mediate renal injury including the innate and adaptive immune systems, the induction of cytokines, chemokines, adhesion molecules as well as interactions with glucocorticoids and the hypothalamic-pituitary-adrenal axis. MIF exerts its biological activities via signaling through its CD74/CD44 receptor complex to activate the downstream ERK1/2 MAP kinase. The functional importance of MIF in kidney disease is demonstrated by the findings that treatment with a neutralizing anti-MIF antibody is able to prevent or reverse renal injury in crescentic anti-GBM glomerulonephritis. In addition, mice null for MIF are protected against immune-mediated lupus nephritis. MIF plays a critical role in kidney diseases and further studies of the functional role and signaling mechanisms of MIF in human kidney diseases are needed.
    Type of Medium: Online Resource
    ISSN: 1660-2129
    URL: Article
    DOI: 10.1159/000145463
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2008
    detail.hit.zdb_id: 2098337-2
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  • 5
    Online Resource
    Online Resource
    Effect of Hexasulfobutylated C〈sub〉60〈/sub〉 on the Isolated Aortic Ring of Guinea Pig
    S. Karger AG ; 2002
    In:  Pharmacology Vol. 64, No. 2 ( 2002), p. 91-97
    Details
    In: Pharmacology, S. Karger AG, Vol. 64, No. 2 ( 2002), p. 91-97
    Abstract: The effects of hexasulfobutylated C 〈 sub 〉 60 〈 /sub 〉 (FC 〈 sub 〉 4 〈 /sub 〉 S) and monomalonic acid C 〈 sub 〉 60 〈 /sub 〉 (MMA C 〈 sub 〉 60 〈 /sub 〉 ), the fullerene C 〈 sub 〉 60 〈 /sub 〉 derivatives, on isolated endothelium-containing or endothelium-denuded aorta of guinea pig were studied pharmacologically in vitro. In the endothelium-containing preparation of the aortic rings, phenylephrine (PHE) elicited contracture and acetylcholine (ACh) elicited a relaxing effect on the PHE-precontracted preparation. In the PHE-precontracted preparation, MMA C 〈 sub 〉 60 〈 /sub 〉 (10 µmol/l) did not elicit a relaxing effect on the PHE-precontracted preparation. However, MMA C 〈 sub 〉 60 〈 /sub 〉 (10 µmol/l) significantly reduced the maximum response of the relaxation elicited by ACh. FC 〈 sub 〉 4 〈 /sub 〉 S itself significantly relaxed the PHE-precontracted aortic rings. ACh-induced relaxation in PHE-precontracted endothelium-containing strips of the aortic rings was significantly potentiated if pretreated with FC 〈 sub 〉 4 〈 /sub 〉 S (10 µmol/l). In the denuded aortic rings, FC 〈 sub 〉 4 〈 /sub 〉 S did not elicit the relaxing effect in the PHE-precontracted preparation. The relaxing effect of FC 〈 sub 〉 4 〈 /sub 〉 S on the PHE-precontracted preparation was not altered when superoxide dismutase (250 units/ml) was pretreated. However, the relaxing effect was reduced when N(G)-nitro- 〈 i 〉 L 〈 /i 〉 -arginine methyl ester ( 〈 i 〉 L 〈 /i 〉 -NAME, 1 mmol/l) or methylene blue (1 µmol/l) was pretreated. These results demonstrated that the vasorelaxation effect of FC 〈 sub 〉 4 〈 /sub 〉 S on the PHE-precontracted aortic ring is partly dependent on the release of nitric oxide (NO) or an NO-derived substance from the vascular endothelium.
    Type of Medium: Online Resource
    ISSN: 0031-7012 , 1423-0313
    URL: Article
    DOI: 10.1159/000056156
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2002
    detail.hit.zdb_id: 1483550-2
    SSG: 15,3
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