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Induction of B7-1 in podocytes is associated with nephrotic syndrome

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Induction of B7-1 in podocytes is associated with nephrotic syndrome. / Reiser, Jochen; von Gersdorff, Gero; Loos, Martin; Oh, Jun; Asanuma, Katsuhiko; Giardino, Laura; Rastaldi, Maria Pia; Calvaresi, Novella; Watanabe, Haruko; Schwarz, Karin; Faul, Christian; Kretzler, Matthias; Davidson, Anne; Sugimoto, Hikaru; Kalluri, Raghu; Sharpe, Arlene H; Kreidberg, Jordan A; Mundel, Peter.

in: J CLIN INVEST, Jahrgang 113, Nr. 10, 05.2004, S. 1390-7.

Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung

Harvard

Reiser, J, von Gersdorff, G, Loos, M, Oh, J, Asanuma, K, Giardino, L, Rastaldi, MP, Calvaresi, N, Watanabe, H, Schwarz, K, Faul, C, Kretzler, M, Davidson, A, Sugimoto, H, Kalluri, R, Sharpe, AH, Kreidberg, JA & Mundel, P 2004, 'Induction of B7-1 in podocytes is associated with nephrotic syndrome', J CLIN INVEST, Jg. 113, Nr. 10, S. 1390-7. https://doi.org/10.1172/JCI20402

APA

Reiser, J., von Gersdorff, G., Loos, M., Oh, J., Asanuma, K., Giardino, L., Rastaldi, M. P., Calvaresi, N., Watanabe, H., Schwarz, K., Faul, C., Kretzler, M., Davidson, A., Sugimoto, H., Kalluri, R., Sharpe, A. H., Kreidberg, J. A., & Mundel, P. (2004). Induction of B7-1 in podocytes is associated with nephrotic syndrome. J CLIN INVEST, 113(10), 1390-7. https://doi.org/10.1172/JCI20402

Vancouver

Reiser J, von Gersdorff G, Loos M, Oh J, Asanuma K, Giardino L et al. Induction of B7-1 in podocytes is associated with nephrotic syndrome. J CLIN INVEST. 2004 Mai;113(10):1390-7. https://doi.org/10.1172/JCI20402

Bibtex

@article{413673589b4740328d68bf59ef56017c,
title = "Induction of B7-1 in podocytes is associated with nephrotic syndrome",
abstract = "Kidney podocytes and their slit diaphragms form the final barrier to urinary protein loss. This explains why podocyte injury is typically associated with nephrotic syndrome. The present study uncovered an unanticipated novel role for costimulatory molecule B7-1 in podocytes as an inducible modifier of glomerular permselectivity. B7-1 in podocytes was found in genetic, drug-induced, immune-mediated, and bacterial toxin-induced experimental kidney diseases with nephrotic syndrome. The clinical significance of our results is underscored by the observation that podocyte expression of B7-1 correlated with the severity of human lupus nephritis. In vivo, exposure to low-dose LPS rapidly upregulates B7-1 in podocytes of WT and SCID mice, leading to nephrotic-range proteinuria. Mice lacking B7-1 are protected from LPS-induced nephrotic syndrome, suggesting a link between podocyte B7-1 expression and proteinuria. LPS signaling through toll-like receptor-4 reorganized the podocyte actin cytoskeleton in vitro, and activation of B7-1 in cultured podocytes led to reorganization of vital slit diaphragm proteins. In summary, upregulation of B7-1 in podocytes may contribute to the pathogenesis of proteinuria by disrupting the glomerular filter and provides a novel molecular target to tackle proteinuric kidney diseases. Our findings suggest a novel function for B7-1 in danger signaling by nonimmune cells.",
keywords = "Actins/metabolism, Animals, B7-1 Antigen/biosynthesis, Base Sequence, DNA/genetics, Humans, In Vitro Techniques, Integrin alpha3/genetics, Kidney/immunology, Lipopolysaccharides/toxicity, Lupus Nephritis/etiology, Membrane Glycoproteins/metabolism, Membrane Proteins, Mice, Mice, Knockout, Mice, SCID, Nephrotic Syndrome/etiology, Proteins/genetics, Receptors, Cell Surface/metabolism, Signal Transduction, Toll-Like Receptor 4, Toll-Like Receptors",
author = "Jochen Reiser and {von Gersdorff}, Gero and Martin Loos and Jun Oh and Katsuhiko Asanuma and Laura Giardino and Rastaldi, {Maria Pia} and Novella Calvaresi and Haruko Watanabe and Karin Schwarz and Christian Faul and Matthias Kretzler and Anne Davidson and Hikaru Sugimoto and Raghu Kalluri and Sharpe, {Arlene H} and Kreidberg, {Jordan A} and Peter Mundel",
year = "2004",
month = may,
doi = "10.1172/JCI20402",
language = "English",
volume = "113",
pages = "1390--7",
journal = "J CLIN INVEST",
issn = "0021-9738",
publisher = "The American Society for Clinical Investigation",
number = "10",

}

RIS

TY - JOUR

T1 - Induction of B7-1 in podocytes is associated with nephrotic syndrome

AU - Reiser, Jochen

AU - von Gersdorff, Gero

AU - Loos, Martin

AU - Oh, Jun

AU - Asanuma, Katsuhiko

AU - Giardino, Laura

AU - Rastaldi, Maria Pia

AU - Calvaresi, Novella

AU - Watanabe, Haruko

AU - Schwarz, Karin

AU - Faul, Christian

AU - Kretzler, Matthias

AU - Davidson, Anne

AU - Sugimoto, Hikaru

AU - Kalluri, Raghu

AU - Sharpe, Arlene H

AU - Kreidberg, Jordan A

AU - Mundel, Peter

PY - 2004/5

Y1 - 2004/5

N2 - Kidney podocytes and their slit diaphragms form the final barrier to urinary protein loss. This explains why podocyte injury is typically associated with nephrotic syndrome. The present study uncovered an unanticipated novel role for costimulatory molecule B7-1 in podocytes as an inducible modifier of glomerular permselectivity. B7-1 in podocytes was found in genetic, drug-induced, immune-mediated, and bacterial toxin-induced experimental kidney diseases with nephrotic syndrome. The clinical significance of our results is underscored by the observation that podocyte expression of B7-1 correlated with the severity of human lupus nephritis. In vivo, exposure to low-dose LPS rapidly upregulates B7-1 in podocytes of WT and SCID mice, leading to nephrotic-range proteinuria. Mice lacking B7-1 are protected from LPS-induced nephrotic syndrome, suggesting a link between podocyte B7-1 expression and proteinuria. LPS signaling through toll-like receptor-4 reorganized the podocyte actin cytoskeleton in vitro, and activation of B7-1 in cultured podocytes led to reorganization of vital slit diaphragm proteins. In summary, upregulation of B7-1 in podocytes may contribute to the pathogenesis of proteinuria by disrupting the glomerular filter and provides a novel molecular target to tackle proteinuric kidney diseases. Our findings suggest a novel function for B7-1 in danger signaling by nonimmune cells.

AB - Kidney podocytes and their slit diaphragms form the final barrier to urinary protein loss. This explains why podocyte injury is typically associated with nephrotic syndrome. The present study uncovered an unanticipated novel role for costimulatory molecule B7-1 in podocytes as an inducible modifier of glomerular permselectivity. B7-1 in podocytes was found in genetic, drug-induced, immune-mediated, and bacterial toxin-induced experimental kidney diseases with nephrotic syndrome. The clinical significance of our results is underscored by the observation that podocyte expression of B7-1 correlated with the severity of human lupus nephritis. In vivo, exposure to low-dose LPS rapidly upregulates B7-1 in podocytes of WT and SCID mice, leading to nephrotic-range proteinuria. Mice lacking B7-1 are protected from LPS-induced nephrotic syndrome, suggesting a link between podocyte B7-1 expression and proteinuria. LPS signaling through toll-like receptor-4 reorganized the podocyte actin cytoskeleton in vitro, and activation of B7-1 in cultured podocytes led to reorganization of vital slit diaphragm proteins. In summary, upregulation of B7-1 in podocytes may contribute to the pathogenesis of proteinuria by disrupting the glomerular filter and provides a novel molecular target to tackle proteinuric kidney diseases. Our findings suggest a novel function for B7-1 in danger signaling by nonimmune cells.

KW - Actins/metabolism

KW - Animals

KW - B7-1 Antigen/biosynthesis

KW - Base Sequence

KW - DNA/genetics

KW - Humans

KW - In Vitro Techniques

KW - Integrin alpha3/genetics

KW - Kidney/immunology

KW - Lipopolysaccharides/toxicity

KW - Lupus Nephritis/etiology

KW - Membrane Glycoproteins/metabolism

KW - Membrane Proteins

KW - Mice

KW - Mice, Knockout

KW - Mice, SCID

KW - Nephrotic Syndrome/etiology

KW - Proteins/genetics

KW - Receptors, Cell Surface/metabolism

KW - Signal Transduction

KW - Toll-Like Receptor 4

KW - Toll-Like Receptors

U2 - 10.1172/JCI20402

DO - 10.1172/JCI20402

M3 - SCORING: Journal article

C2 - 15146236

VL - 113

SP - 1390

EP - 1397

JO - J CLIN INVEST

JF - J CLIN INVEST

SN - 0021-9738

IS - 10

ER -