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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response

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Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response. / Schell, Christoph; Kretz, Oliver; Bregenzer, Andreas; Rogg, Manuel; Helmstädter, Martin; Lisewski, Ulrike; Gotthardt, Michael; Tharaux, Pierre-Louis; Huber, Tobias B; Grahammer, Florian.

In: PLOS ONE, Vol. 10, No. 6, 2015, p. e0129424.

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

Harvard

Schell, C, Kretz, O, Bregenzer, A, Rogg, M, Helmstädter, M, Lisewski, U, Gotthardt, M, Tharaux, P-L, Huber, TB & Grahammer, F 2015, 'Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response', PLOS ONE, vol. 10, no. 6, pp. e0129424. https://doi.org/10.1371/journal.pone.0129424

APA

Schell, C., Kretz, O., Bregenzer, A., Rogg, M., Helmstädter, M., Lisewski, U., Gotthardt, M., Tharaux, P-L., Huber, T. B., & Grahammer, F. (2015). Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response. PLOS ONE, 10(6), e0129424. https://doi.org/10.1371/journal.pone.0129424

Vancouver

Schell C, Kretz O, Bregenzer A, Rogg M, Helmstädter M, Lisewski U et al. Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response. PLOS ONE. 2015;10(6):e0129424. https://doi.org/10.1371/journal.pone.0129424

Bibtex

@article{8d5e28d9daf84a0787d7a41dcfcd5e2d,
title = "Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response",
abstract = "The coxsackie- and adenovirus receptor (CXADR) is a member of the immunoglobulin protein superfamily, present in various epithelial cells including glomerular epithelial cells. Beside its known function as a virus receptor, it also constitutes an integral part of cell-junctions. Previous studies in the zebrafish pronephros postulated a potential role of CXADR for the terminal differentiation of glomerular podocytes and correct patterning of the elaborated foot process architecture. However, due to early embryonic lethality of constitutive Cxadr knockout mice, mammalian data on kidney epithelial cells have been lacking. Interestingly, Cxadr is robustly expressed during podocyte development and in adulthood in response to glomerular injury. We therefore used a conditional transgenic approach to elucidate the function of Cxadr for podocyte development and stress response. Surprisingly, we could not discern a developmental phenotype in podocyte specific Cxadr knock-out mice. In addition, despite a significant up regulation of CXADR during toxic, genetic and immunologic podocyte injury, we could not detect any impact of Cxadr on these injury models. Thus these data indicate that in contrast to lower vertebrate models, mammalian podocytes have acquired molecular programs to compensate for the loss of Cxadr.",
keywords = "Animals, Coxsackie and Adenovirus Receptor-Like Membrane Protein, Gene Deletion, Gene Expression, Gene Knockout Techniques, Kidney, Kidney Glomerulus, Mice, Mice, Knockout, Podocytes, Stress, Physiological, Journal Article, Research Support, Non-U.S. Gov't",
author = "Christoph Schell and Oliver Kretz and Andreas Bregenzer and Manuel Rogg and Martin Helmst{\"a}dter and Ulrike Lisewski and Michael Gotthardt and Pierre-Louis Tharaux and Huber, {Tobias B} and Florian Grahammer",
year = "2015",
doi = "10.1371/journal.pone.0129424",
language = "English",
volume = "10",
pages = "e0129424",
journal = "PLOS ONE",
issn = "1932-6203",
publisher = "Public Library of Science",
number = "6",

}

RIS

TY - JOUR

T1 - Podocyte-Specific Deletion of Murine CXADR Does Not Impair Podocyte Development, Function or Stress Response

AU - Schell, Christoph

AU - Kretz, Oliver

AU - Bregenzer, Andreas

AU - Rogg, Manuel

AU - Helmstädter, Martin

AU - Lisewski, Ulrike

AU - Gotthardt, Michael

AU - Tharaux, Pierre-Louis

AU - Huber, Tobias B

AU - Grahammer, Florian

PY - 2015

Y1 - 2015

N2 - The coxsackie- and adenovirus receptor (CXADR) is a member of the immunoglobulin protein superfamily, present in various epithelial cells including glomerular epithelial cells. Beside its known function as a virus receptor, it also constitutes an integral part of cell-junctions. Previous studies in the zebrafish pronephros postulated a potential role of CXADR for the terminal differentiation of glomerular podocytes and correct patterning of the elaborated foot process architecture. However, due to early embryonic lethality of constitutive Cxadr knockout mice, mammalian data on kidney epithelial cells have been lacking. Interestingly, Cxadr is robustly expressed during podocyte development and in adulthood in response to glomerular injury. We therefore used a conditional transgenic approach to elucidate the function of Cxadr for podocyte development and stress response. Surprisingly, we could not discern a developmental phenotype in podocyte specific Cxadr knock-out mice. In addition, despite a significant up regulation of CXADR during toxic, genetic and immunologic podocyte injury, we could not detect any impact of Cxadr on these injury models. Thus these data indicate that in contrast to lower vertebrate models, mammalian podocytes have acquired molecular programs to compensate for the loss of Cxadr.

AB - The coxsackie- and adenovirus receptor (CXADR) is a member of the immunoglobulin protein superfamily, present in various epithelial cells including glomerular epithelial cells. Beside its known function as a virus receptor, it also constitutes an integral part of cell-junctions. Previous studies in the zebrafish pronephros postulated a potential role of CXADR for the terminal differentiation of glomerular podocytes and correct patterning of the elaborated foot process architecture. However, due to early embryonic lethality of constitutive Cxadr knockout mice, mammalian data on kidney epithelial cells have been lacking. Interestingly, Cxadr is robustly expressed during podocyte development and in adulthood in response to glomerular injury. We therefore used a conditional transgenic approach to elucidate the function of Cxadr for podocyte development and stress response. Surprisingly, we could not discern a developmental phenotype in podocyte specific Cxadr knock-out mice. In addition, despite a significant up regulation of CXADR during toxic, genetic and immunologic podocyte injury, we could not detect any impact of Cxadr on these injury models. Thus these data indicate that in contrast to lower vertebrate models, mammalian podocytes have acquired molecular programs to compensate for the loss of Cxadr.

KW - Animals

KW - Coxsackie and Adenovirus Receptor-Like Membrane Protein

KW - Gene Deletion

KW - Gene Expression

KW - Gene Knockout Techniques

KW - Kidney

KW - Kidney Glomerulus

KW - Mice

KW - Mice, Knockout

KW - Podocytes

KW - Stress, Physiological

KW - Journal Article

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

U2 - 10.1371/journal.pone.0129424

DO - 10.1371/journal.pone.0129424

M3 - SCORING: Journal article

C2 - 26076477

VL - 10

SP - e0129424

JO - PLOS ONE

JF - PLOS ONE

SN - 1932-6203

IS - 6

ER -