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Wnt pathway regulation in chronic renal allograft damage

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Wnt pathway regulation in chronic renal allograft damage. / von Toerne, C; Schmidt, C; Adams, J; Kiss, E; Bedke, J; Porubsky, S; Gretz, N; Lindenmeyer, M T; Cohen, C D; Gröne, H-J; Nelson, P J.

In: AM J TRANSPLANT, Vol. 9, No. 10, 10.2009, p. 2223-39.

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

Harvard

von Toerne, C, Schmidt, C, Adams, J, Kiss, E, Bedke, J, Porubsky, S, Gretz, N, Lindenmeyer, MT, Cohen, CD, Gröne, H-J & Nelson, PJ 2009, 'Wnt pathway regulation in chronic renal allograft damage', AM J TRANSPLANT, vol. 9, no. 10, pp. 2223-39. https://doi.org/10.1111/j.1600-6143.2009.02762.x

APA

von Toerne, C., Schmidt, C., Adams, J., Kiss, E., Bedke, J., Porubsky, S., Gretz, N., Lindenmeyer, M. T., Cohen, C. D., Gröne, H-J., & Nelson, P. J. (2009). Wnt pathway regulation in chronic renal allograft damage. AM J TRANSPLANT, 9(10), 2223-39. https://doi.org/10.1111/j.1600-6143.2009.02762.x

Vancouver

von Toerne C, Schmidt C, Adams J, Kiss E, Bedke J, Porubsky S et al. Wnt pathway regulation in chronic renal allograft damage. AM J TRANSPLANT. 2009 Oct;9(10):2223-39. https://doi.org/10.1111/j.1600-6143.2009.02762.x

Bibtex

@article{de9f28da9a284ab8ab35ef6e821b92b2,
title = "Wnt pathway regulation in chronic renal allograft damage",
abstract = "The Wnt signaling pathway, linked to development, has been proposed to be recapitulated during the progressive damage associated with chronic organ failure. Chronic allograft damage following kidney transplantation is characterized by progressive fibrosis and a smoldering inflammatory infiltrate. A modified, Fischer 344 (RT1(lvl)) to Lewis (RT1(l)) rat renal allograft model that reiterates many of the major pathophysiologic processes seen in patients with chronic allograft failure was used to study the progressive disease phenotype and specific gene product expression by immunohistochemistry and transcriptomic profiling. Central components of the Tgfb, canonical Wnt and Wnt-Ca2+ signaling pathways were significantly altered with the development of chronic damage. In the canonical Wnt pathway, Wnt3, Lef1 and Tcf1 showed differential regulation. Target genes Fn1, Cd44, Mmp7 and Nos2 were upregulated and associated with the progression of renal damage. Changes in the Wnt-Ca2+ pathway were evidenced by increased expression of Wnt6, Wnt7a, protein kinase C, Cam Kinase II and Nfat transcription factors and the target gene vimentin. No evidence for alterations in the Wnt planar cell polarity (PCP) pathway was detected. Overall results suggest cross talk between the Wnt and Tgfb signaling pathways during allograft inflammatory damage and present potential targets for therapeutic intervention.",
keywords = "Animals, Cell Differentiation, Cell Polarity, Fibrosis, Gene Expression Profiling, Immunohistochemistry, Kidney, Kidney Transplantation, Male, Models, Animal, Polymerase Chain Reaction, RNA, Messenger, Rats, Rats, Inbred F344, Rats, Inbred Lew, Signal Transduction, Transplantation, Homologous, Wnt Proteins, Journal Article, Research Support, Non-U.S. Gov't",
author = "{von Toerne}, C and C Schmidt and J Adams and E Kiss and J Bedke and S Porubsky and N Gretz and Lindenmeyer, {M T} and Cohen, {C D} and H-J Gr{\"o}ne and Nelson, {P J}",
year = "2009",
month = oct,
doi = "10.1111/j.1600-6143.2009.02762.x",
language = "English",
volume = "9",
pages = "2223--39",
journal = "AM J TRANSPLANT",
issn = "1600-6135",
publisher = "Wiley-Blackwell",
number = "10",

}

RIS

TY - JOUR

T1 - Wnt pathway regulation in chronic renal allograft damage

AU - von Toerne, C

AU - Schmidt, C

AU - Adams, J

AU - Kiss, E

AU - Bedke, J

AU - Porubsky, S

AU - Gretz, N

AU - Lindenmeyer, M T

AU - Cohen, C D

AU - Gröne, H-J

AU - Nelson, P J

PY - 2009/10

Y1 - 2009/10

N2 - The Wnt signaling pathway, linked to development, has been proposed to be recapitulated during the progressive damage associated with chronic organ failure. Chronic allograft damage following kidney transplantation is characterized by progressive fibrosis and a smoldering inflammatory infiltrate. A modified, Fischer 344 (RT1(lvl)) to Lewis (RT1(l)) rat renal allograft model that reiterates many of the major pathophysiologic processes seen in patients with chronic allograft failure was used to study the progressive disease phenotype and specific gene product expression by immunohistochemistry and transcriptomic profiling. Central components of the Tgfb, canonical Wnt and Wnt-Ca2+ signaling pathways were significantly altered with the development of chronic damage. In the canonical Wnt pathway, Wnt3, Lef1 and Tcf1 showed differential regulation. Target genes Fn1, Cd44, Mmp7 and Nos2 were upregulated and associated with the progression of renal damage. Changes in the Wnt-Ca2+ pathway were evidenced by increased expression of Wnt6, Wnt7a, protein kinase C, Cam Kinase II and Nfat transcription factors and the target gene vimentin. No evidence for alterations in the Wnt planar cell polarity (PCP) pathway was detected. Overall results suggest cross talk between the Wnt and Tgfb signaling pathways during allograft inflammatory damage and present potential targets for therapeutic intervention.

AB - The Wnt signaling pathway, linked to development, has been proposed to be recapitulated during the progressive damage associated with chronic organ failure. Chronic allograft damage following kidney transplantation is characterized by progressive fibrosis and a smoldering inflammatory infiltrate. A modified, Fischer 344 (RT1(lvl)) to Lewis (RT1(l)) rat renal allograft model that reiterates many of the major pathophysiologic processes seen in patients with chronic allograft failure was used to study the progressive disease phenotype and specific gene product expression by immunohistochemistry and transcriptomic profiling. Central components of the Tgfb, canonical Wnt and Wnt-Ca2+ signaling pathways were significantly altered with the development of chronic damage. In the canonical Wnt pathway, Wnt3, Lef1 and Tcf1 showed differential regulation. Target genes Fn1, Cd44, Mmp7 and Nos2 were upregulated and associated with the progression of renal damage. Changes in the Wnt-Ca2+ pathway were evidenced by increased expression of Wnt6, Wnt7a, protein kinase C, Cam Kinase II and Nfat transcription factors and the target gene vimentin. No evidence for alterations in the Wnt planar cell polarity (PCP) pathway was detected. Overall results suggest cross talk between the Wnt and Tgfb signaling pathways during allograft inflammatory damage and present potential targets for therapeutic intervention.

KW - Animals

KW - Cell Differentiation

KW - Cell Polarity

KW - Fibrosis

KW - Gene Expression Profiling

KW - Immunohistochemistry

KW - Kidney

KW - Kidney Transplantation

KW - Male

KW - Models, Animal

KW - Polymerase Chain Reaction

KW - RNA, Messenger

KW - Rats

KW - Rats, Inbred F344

KW - Rats, Inbred Lew

KW - Signal Transduction

KW - Transplantation, Homologous

KW - Wnt Proteins

KW - Journal Article

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

U2 - 10.1111/j.1600-6143.2009.02762.x

DO - 10.1111/j.1600-6143.2009.02762.x

M3 - SCORING: Journal article

C2 - 19681821

VL - 9

SP - 2223

EP - 2239

JO - AM J TRANSPLANT

JF - AM J TRANSPLANT

SN - 1600-6135

IS - 10

ER -