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  • 1
    Online Resource
    Online Resource
    Activated Renal Macrophages Are Markers of Disease Onset and Disease Remission in Lupus Nephritis
    The American Association of Immunologists ; 2008
    In:  The Journal of Immunology Vol. 180, No. 3 ( 2008-02-01), p. 1938-1947
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 180, No. 3 ( 2008-02-01), p. 1938-1947
    Abstract: Costimulatory blockade with CTLA4Ig and anti-CD40L along with a single dose of cyclophosphamide induces remission of systemic lupus erythematosus nephritis in NZB/W F1 mice. To understand the mechanisms for remission and for impending relapse, we examined the expression profiles of 61 inflammatory molecules in the perfused kidneys of treated mice and untreated mice at different stages of disease. Further studies using flow cytometry and immunohistochemistry allowed us to determine the cellular origins of several key markers. We show that only a limited set of inflammatory mediators is expressed in the kidney following glomerular immune complex deposition but before the onset of proteinuria. Formation of a lymphoid aggregate in the renal pelvis precedes the invasion of the kidney by inflammatory cells. Regulatory molecules are expressed early in the disease process and during remission but do not prevent the inevitable progression of active inflammation. Onset of proliferative glomerulonephritis and proteinuria is associated with activation of the renal endothelium, expression of chemokines that mediate glomerular cell infiltration, and infiltration by activated dendritic cells and macrophages that migrate to different topographical areas of the kidney but express a similar profile of inflammatory cytokines. Increasing interstitial infiltration by macrophages and progressive tubular damage, manifested by production of lipocalin-2, occur later in the disease process. Studies of treated mice identify a type II (M2b)-activated macrophage as a marker of remission induction and impending relapse and suggest that therapy for systemic lupus erythematosus nephritis should include strategies that prevent both activation of monocytes and their migration to the kidney.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.180.3.1938
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2008
    detail.hit.zdb_id: 1475085-5
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  • 2
    Online Resource
    Online Resource
    IGF-Binding Protein-3 Modulates TGF-β/BMP-Signaling in Glomerular Podocytes
    Ovid Technologies (Wolters Kluwer Health) ; 2006
    In:  Journal of the American Society of Nephrology Vol. 17, No. 6 ( 2006-06), p. 1644-1656
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 17, No. 6 ( 2006-06), p. 1644-1656
    Type of Medium: Online Resource
    ISSN: 1046-6673
    URL: Article
    DOI: 10.1681/ASN.2005111209
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
    detail.hit.zdb_id: 2029124-3
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  • 3
    Online Resource
    Online Resource
    Leptin is a coactivator of TGF-β in unilateral ureteral obstructive kidney disease
    American Physiological Society ; 2007
    In:  American Journal of Physiology-Renal Physiology Vol. 293, No. 4 ( 2007-10), p. F1355-F1362
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 293, No. 4 ( 2007-10), p. F1355-F1362
    Abstract: Progressive tubulointerstitial fibrosis is the common end point leading to end-stage renal disease in experimental and clinical settings. Since the peptide hormone leptin is involved not only in the regulation of obesity but also in the regulation of inflammation and fibrosis, we tested the hypothesis whether leptin deficiency has an impact on tubulointerstitial fibrosis in mice. Leptin-deficient ( ob/ ob) and leptin receptor-deficient mice ( db/ db) were exposed to 14 days of unilateral ureteral obstruction (UUO). The degree of fibrosis and inflammation was compared with that in sham-operated mice by performing immunohistochemistry, quantitative PCR, and Western blotting. We found that tubulointerstitial fibrosis was significantly reduced in the obstructed kidneys of ob/ ob compared with db/ db mice or control mice. Detailed analysis of infiltrating inflammatory cells by immunohistochemistry revealed a significant reduction of CD4 + cells at 14 days after UUO in both ob/ ob and db/ db mice. In contrast, we could not detect significant differences in CD8 + cells and macrophage content. Transforming growth factor (TGF)-β mRNA levels, TGF-β-induced Smad-2/3 activation, and the upregulation of downstream target genes were significantly reduced in ob/ ob mice. In addition, we demonstrated that leptin could enhance TGF-β signaling in normal rat kidney fibroblasts in vitro. We conclude that leptin can serve as a cofactor of TGF-β activation and thus plays an important role in renal tubulointerstitial fibrosis. Therefore, selective blockade of the leptin axis might provide a therapeutic possibility to prevent or delay fibrotic kidney disease.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00003.2007
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2007
    detail.hit.zdb_id: 1477287-5
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  • 4
    Online Resource
    Online Resource
    The balance of autocrine VEGF-A and VEGF-C determines podocyte survival
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Renal Physiology Vol. 297, No. 6 ( 2009-12), p. F1656-F1667
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 297, No. 6 ( 2009-12), p. F1656-F1667
    Abstract: Podocytes are an important component of the glomerular filtration barrier and are the major source of vascular endothelial growth factor (VEGF) in the glomerulus. The role of VEGF for the phenotype of the glomerular endothelium has been intensely studied; however, the direct effects of autocrine VEGF on the podocyte are largely unknown. In this study we characterized the expression of VEGF isoforms and VEGF receptors in cultured human podocytes and examined direct effects on cell signaling and apoptosis after stimulation with exogenous VEGF or ablation of autocrine VEGF. We identified VEGF-A and VEGF-C as the dominant isoforms in human podocytes and showed that autocrine levels of both are important for the intracellular activation of antiapoptotic phosphoinositol 3-kinase/AKT and suppression of the proapoptotic p38MAPK via VEGFR-2. We demonstrated that ablation of VEGF-A or VEGF-C as well as treatment with bevacizumab or a VEGFR-2/-3 tyrosine kinase inhibitor led to reduced podocyte survival. In contrast, ablation of VEGF-B had no effect on podocyte survival. Treatment with exogenous VEGF-C reversed the effect of VEGF-A neutralization, and exogenous VEGF-A abrogated the effect of VEGF-C ablation in human podocytes. Our results underline the importance of autocrine VEGF for podocyte survival and indicate the delicate balance of VEGF-A and VEGF-C to influence progression of glomerular diseases.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.00275.2009
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477287-5
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  • 5
    Online Resource
    Online Resource
    Evaluation of Urine Proteome Pattern Analysis for Its Potential To Reflect Coronary Artery Atherosclerosis in Symptomatic Patients
    American Chemical Society (ACS) ; 2009
    In:  Journal of Proteome Research Vol. 8, No. 1 ( 2009-01-02), p. 335-345
    Details
    In: Journal of Proteome Research, American Chemical Society (ACS), Vol. 8, No. 1 ( 2009-01-02), p. 335-345
    Type of Medium: Online Resource
    ISSN: 1535-3893 , 1535-3907
    URL: Article
    DOI: 10.1021/pr800615t
    Language: English
    Publisher: American Chemical Society (ACS)
    Publication Date: 2009
    detail.hit.zdb_id: 2065254-9
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    CD2AP/CIN85 Balance Determines Receptor Tyrosine Kinase Signaling Response in Podocytes
    Elsevier BV ; 2007
    In:  Journal of Biological Chemistry Vol. 282, No. 10 ( 2007-03), p. 7457-7464
    Details
    In: Journal of Biological Chemistry, Elsevier BV, Vol. 282, No. 10 ( 2007-03), p. 7457-7464
    Type of Medium: Online Resource
    ISSN: 0021-9258
    URL: Article
    DOI: 10.1074/jbc.M608519200
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2007
    detail.hit.zdb_id: 2141744-1
    detail.hit.zdb_id: 1474604-9
    SSG: 12
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  • 7
    Online Resource
    Online Resource
    Glomerular epithelial cells in the urine: what has to be done to make them worthwhile?
    American Physiological Society ; 2009
    In:  American Journal of Physiology-Renal Physiology Vol. 296, No. 2 ( 2009-02), p. F230-F241
    Details
    In: American Journal of Physiology-Renal Physiology, American Physiological Society, Vol. 296, No. 2 ( 2009-02), p. F230-F241
    Abstract: The significance of the native urine sediment in the differential of glomerular diseases needs no further comment. However, the question arises whether it could be useful to develop a more specific diagnostic approach to identify the origin of renal epithelial cells that can be detected in the urine sediments as well. Especially the detection of podocytes in the urine could be a valuable noninvasive method to get information about the disease activity or disease type and could be used as a follow-up after a biopsy in an outpatient setting. So far, there are only a few studies that analyzed the clinical relevance of renal epithelial cells in the urine systematically or prospectively. The reason for this could be the nature of the material since it will remain unclear whether detachment and changes in the urine milieu have a direct effect on the expression of marker proteins on the detected cells. Dedifferentiation or transdifferentiation of cells that goes along with changed marker expression is certainly also part of the underlying disease process. This review summarizes the available information on marker proteins that have been successfully used in the diagnostic of “podocytes” in the urine. Furthermore, it gives an overview of marker expression on podocytes in situ in development and disease and examines the role of glomerular epithelial shedding in the urine at the interface of basic science and clinical medicine.
    Type of Medium: Online Resource
    ISSN: 1931-857X , 1522-1466
    URL: Article
    DOI: 10.1152/ajprenal.90507.2008
    Language: English
    Publisher: American Physiological Society
    Publication Date: 2009
    detail.hit.zdb_id: 1477287-5
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  • 8
    Online Resource
    Online Resource
    Determination of N -Desmethyl- and N -Bisdesmethyl Metabolites of Sibutramine in Doping Control Analysis Using Liquid Chromatography-Tandem Mass Spectrometry
    SAGE Publications ; 2006
    In:  European Journal of Mass Spectrometry Vol. 12, No. 2 ( 2006-04), p. 129-136
    Details
    In: European Journal of Mass Spectrometry, SAGE Publications, Vol. 12, No. 2 ( 2006-04), p. 129-136
    Abstract: Since January 2006, the list of prohibited substances established by the World Anti-Doping Agency includes the antidepressant/anti-obesity drug Sibutramine. Due to its rapid degradation to its active metabolites N-desmethyl and N-bisdesmethyl sibutramine, reference compounds were synthesized and included into an existing screening assay to allow the unambiguous determination of these metabolic products in human urine using liquid–liquid extraction followed by liquid chromatography/tandem mass spectrometry. Characteristic product ions, obtained after electrospray ionization and collision-induced dissociation, were elucidated using high resolution/high accuracy mass measurements with a hybrid linear ion trap/orbitrap mass analyzer. Based on diagnostic product ions, the extended screening procedure was validated for both sibutramine metabolites using a triple quadrupole mass spectrometer. Items such as lower limits of detection (6–40 ng mL −1 ), recoveries (39–42%), intraday precision (low: 5.5–10.6%, medium: 4.9–5.9%), high: 12.8–16.4%) and interday precision (low: 15.0–22.8%, medium: 17.7–18.6%), high: 16.5–25.6%) were evaluated and a clinical spot urine sample was analyzed to demonstrate the applicability of the developed assay in sports drug testing.
    Type of Medium: Online Resource
    ISSN: 1469-0667 , 1751-6838
    URL: Article
    DOI: 10.1255/ejms.797
    Language: English
    Publisher: SAGE Publications
    Publication Date: 2006
    detail.hit.zdb_id: 2021540-X
    detail.hit.zdb_id: 2021340-2
    SSG: 11
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Erythropoietin Prevents Diabetes-Induced Podocyte Damage
    S. Karger AG ; 2008
    In:  Kidney and Blood Pressure Research Vol. 31, No. 6 ( 2008), p. 411-415
    Details
    In: Kidney and Blood Pressure Research, S. Karger AG, Vol. 31, No. 6 ( 2008), p. 411-415
    Abstract: 〈 i 〉 Objective: 〈 /i 〉 Erythropoietin (EPO) has cytoprotective effects apart from its hematopoietic effects. We studied the effects of different EPO molecules on podocyte signaling in vitro and on podocyte survival in an experimental model of diabetic kidney injury (db/db mouse). 〈 i 〉 Methods: 〈 /i 〉 We elucidated intracellular signaling by epoetin-β, darbepoetin-α, and the continuous erythropoietin receptor activator (CERA) in immortalized murine podocyte cultures. Moreover, we treated db/db micewith placebo or with CERA in a chronic (14-week) randomized controlled study. We also studied non-diabetic db/m mice as controls. 〈 i 〉 Results: 〈 /i 〉 We could clearly demonstrate phosphorylation of the JAK/PI3K pathway and Akt signaling in podocytes by epoetin-β, darbepoetin-α and CERA. In the long-term animal study we found significantly reduced podocyte numbers in placebo-treated db/db mice compared to db/m control mice (7.4 ± 0.2 vs. 10.2 ± 0.9 per glomerular field; p 〈 0.05). Chronic CERA treatment ameliorated podocyte loss in kidneys of diabetic animals (8.5 ± 0.5 per glomerular field; p 〈 0.05 vs. placebo-treated db/db mice). 〈 i 〉 Conclusion: 〈 /i 〉 EPO activates pro-survival intracellular pathways in podocytes in vitro, and ameliorates diabetes-induced podocyte loss in vivo. Chronic EPO administration may be a feasible way to protect podocyte from diabetic injury.
    Type of Medium: Online Resource
    ISSN: 1420-4096 , 1423-0143
    URL: Article
    DOI: 10.1159/000186368
    Language: English
    Publisher: S. Karger AG
    Publication Date: 2008
    detail.hit.zdb_id: 1482922-8
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  • 10
    Online Resource
    Online Resource
    TβRI Independently Activates Smad- and CD2AP-Dependent Pathways in Podocytes
    Ovid Technologies (Wolters Kluwer Health) ; 2009
    In:  Journal of the American Society of Nephrology Vol. 20, No. 10 ( 2009-10), p. 2127-2137
    Details
    In: Journal of the American Society of Nephrology, Ovid Technologies (Wolters Kluwer Health), Vol. 20, No. 10 ( 2009-10), p. 2127-2137
    Type of Medium: Online Resource
    ISSN: 1046-6673
    URL: Article
    DOI: 10.1681/ASN.2008070806
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2009
    detail.hit.zdb_id: 2029124-3
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