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Expression and function of C/EBP homology protein (GADD153) in podocytes

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Expression and function of C/EBP homology protein (GADD153) in podocytes. / Bek, Martin F; Bayer, Michael; Müller, Barbara; Greiber, Stefan; Lang, Detlef; Schwab, Albrecht; August, Christian; Springer, Erik; Rohrbach, Rolf; Huber, Tobias B; Benzing, Thomas; Pavenstädt, Hermann.

In: AM J PATHOL, Vol. 168, No. 1, 01.2006, p. 20-32.

Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review

Harvard

Bek, MF, Bayer, M, Müller, B, Greiber, S, Lang, D, Schwab, A, August, C, Springer, E, Rohrbach, R, Huber, TB, Benzing, T & Pavenstädt, H 2006, 'Expression and function of C/EBP homology protein (GADD153) in podocytes', AM J PATHOL, vol. 168, no. 1, pp. 20-32. https://doi.org/10.2353/ajpath.2006.040774

APA

Bek, M. F., Bayer, M., Müller, B., Greiber, S., Lang, D., Schwab, A., August, C., Springer, E., Rohrbach, R., Huber, T. B., Benzing, T., & Pavenstädt, H. (2006). Expression and function of C/EBP homology protein (GADD153) in podocytes. AM J PATHOL, 168(1), 20-32. https://doi.org/10.2353/ajpath.2006.040774

Vancouver

Bek MF, Bayer M, Müller B, Greiber S, Lang D, Schwab A et al. Expression and function of C/EBP homology protein (GADD153) in podocytes. AM J PATHOL. 2006 Jan;168(1):20-32. https://doi.org/10.2353/ajpath.2006.040774

Bibtex

@article{42995076000946878503d94ebea8ef11,
title = "Expression and function of C/EBP homology protein (GADD153) in podocytes",
abstract = "Podocytes are crucial for the permeability of the glomerular filtration barrier. In glomerular disease, however, reactive oxygen species (ROS) may be involved in podocyte injury and subsequent proteinuria. Here, we describe ROS-dependent gene induction in differentiated podocytes stimulated with H(2)O(2) or xanthine/xanthine-oxidase. Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein). Cultured podocytes overexpressing CHOP showed increased generation of superoxide anions compared to controls. In addition, the expression of alpha(3)/beta(1) integrins, crucial for cell-matrix interaction of podocytes, was down-regulated, leading to increased cell-matrix adhesion and cell displacement. The altered cell-matrix adhesion was antagonized by the ROS scavenger 1,3-dimethyl-2-thiourea, and the increase in cell displacement could be mimicked by stimulating untransfected podocytes with puromycin, an inductor of ROS. We next performed immunohistochemical staining of human kidney tissue (normal, membranous nephropathy, focal segmental glomerulosclerosis, and minimal change nephropathy) as well as sections from rats with puromycin nephrosis, a model of minimal change nephropathy. CHOP was weakly expressed in podocytes of control kidneys but up-regulated in most proteinuric human kidneys and in rat puromycin nephrosis. Our data suggest that CHOP-via increased ROS generation-regulates cell-matrix adhesion of podocytes in glomerular disease.",
keywords = "Animals, Blotting, Western, Cell Adhesion, Cells, Cultured, Disease Models, Animal, Down-Regulation, Free Radical Scavengers, Gene Expression, Humans, Hydrogen Peroxide, Immunohistochemistry, Integrin alpha Chains, Integrin beta Chains, Kidney Diseases, Mice, Podocytes, Polymerase Chain Reaction, RNA, Messenger, RNA, Small Nucleolar, Rats, Reactive Oxygen Species, Superoxides, Transcription Factor CHOP, Journal Article, Research Support, Non-U.S. Gov't",
author = "Bek, {Martin F} and Michael Bayer and Barbara M{\"u}ller and Stefan Greiber and Detlef Lang and Albrecht Schwab and Christian August and Erik Springer and Rolf Rohrbach and Huber, {Tobias B} and Thomas Benzing and Hermann Pavenst{\"a}dt",
year = "2006",
month = jan,
doi = "10.2353/ajpath.2006.040774",
language = "English",
volume = "168",
pages = "20--32",
journal = "AM J PATHOL",
issn = "0002-9440",
publisher = "Elsevier Inc.",
number = "1",

}

RIS

TY - JOUR

T1 - Expression and function of C/EBP homology protein (GADD153) in podocytes

AU - Bek, Martin F

AU - Bayer, Michael

AU - Müller, Barbara

AU - Greiber, Stefan

AU - Lang, Detlef

AU - Schwab, Albrecht

AU - August, Christian

AU - Springer, Erik

AU - Rohrbach, Rolf

AU - Huber, Tobias B

AU - Benzing, Thomas

AU - Pavenstädt, Hermann

PY - 2006/1

Y1 - 2006/1

N2 - Podocytes are crucial for the permeability of the glomerular filtration barrier. In glomerular disease, however, reactive oxygen species (ROS) may be involved in podocyte injury and subsequent proteinuria. Here, we describe ROS-dependent gene induction in differentiated podocytes stimulated with H(2)O(2) or xanthine/xanthine-oxidase. Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein). Cultured podocytes overexpressing CHOP showed increased generation of superoxide anions compared to controls. In addition, the expression of alpha(3)/beta(1) integrins, crucial for cell-matrix interaction of podocytes, was down-regulated, leading to increased cell-matrix adhesion and cell displacement. The altered cell-matrix adhesion was antagonized by the ROS scavenger 1,3-dimethyl-2-thiourea, and the increase in cell displacement could be mimicked by stimulating untransfected podocytes with puromycin, an inductor of ROS. We next performed immunohistochemical staining of human kidney tissue (normal, membranous nephropathy, focal segmental glomerulosclerosis, and minimal change nephropathy) as well as sections from rats with puromycin nephrosis, a model of minimal change nephropathy. CHOP was weakly expressed in podocytes of control kidneys but up-regulated in most proteinuric human kidneys and in rat puromycin nephrosis. Our data suggest that CHOP-via increased ROS generation-regulates cell-matrix adhesion of podocytes in glomerular disease.

AB - Podocytes are crucial for the permeability of the glomerular filtration barrier. In glomerular disease, however, reactive oxygen species (ROS) may be involved in podocyte injury and subsequent proteinuria. Here, we describe ROS-dependent gene induction in differentiated podocytes stimulated with H(2)O(2) or xanthine/xanthine-oxidase. Superoxide anions and H(2)O(2) increased mRNA and protein expression of GAS5 (growth arrest-specific protein 5) and CHOP (C/EBP homology protein). Cultured podocytes overexpressing CHOP showed increased generation of superoxide anions compared to controls. In addition, the expression of alpha(3)/beta(1) integrins, crucial for cell-matrix interaction of podocytes, was down-regulated, leading to increased cell-matrix adhesion and cell displacement. The altered cell-matrix adhesion was antagonized by the ROS scavenger 1,3-dimethyl-2-thiourea, and the increase in cell displacement could be mimicked by stimulating untransfected podocytes with puromycin, an inductor of ROS. We next performed immunohistochemical staining of human kidney tissue (normal, membranous nephropathy, focal segmental glomerulosclerosis, and minimal change nephropathy) as well as sections from rats with puromycin nephrosis, a model of minimal change nephropathy. CHOP was weakly expressed in podocytes of control kidneys but up-regulated in most proteinuric human kidneys and in rat puromycin nephrosis. Our data suggest that CHOP-via increased ROS generation-regulates cell-matrix adhesion of podocytes in glomerular disease.

KW - Animals

KW - Blotting, Western

KW - Cell Adhesion

KW - Cells, Cultured

KW - Disease Models, Animal

KW - Down-Regulation

KW - Free Radical Scavengers

KW - Gene Expression

KW - Humans

KW - Hydrogen Peroxide

KW - Immunohistochemistry

KW - Integrin alpha Chains

KW - Integrin beta Chains

KW - Kidney Diseases

KW - Mice

KW - Podocytes

KW - Polymerase Chain Reaction

KW - RNA, Messenger

KW - RNA, Small Nucleolar

KW - Rats

KW - Reactive Oxygen Species

KW - Superoxides

KW - Transcription Factor CHOP

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.2353/ajpath.2006.040774

DO - 10.2353/ajpath.2006.040774

M3 - SCORING: Journal article

C2 - 16400006

VL - 168

SP - 20

EP - 32

JO - AM J PATHOL

JF - AM J PATHOL

SN - 0002-9440

IS - 1

ER -