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, Jahrgang 10, Nr. 6, 2015, S. e0129424.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Zeitschriftenaufsatz › Forschung › Begutachtung
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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 -