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231225s2018 xx |||||o 00| ||eng c |
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|a 10.1016/j.clim.2018.07.002
|2 doi
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|a pubmed24n0955.xml
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|a (DE-627)NLM286588374
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|a (NLM)30018024
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|a (PII)S1521-6616(18)30389-9
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|a DE-627
|b ger
|c DE-627
|e rakwb
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|a eng
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| 100 |
1 |
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|a Gibbert, Lydia
|e verfasserin
|4 aut
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| 245 |
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|a YB-1 increases glomerular, but decreases interstitial fibrosis in CNI-induced nephropathy
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|c 2018
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|a Text
|b txt
|2 rdacontent
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|a ƒaComputermedien
|b c
|2 rdamedia
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|a ƒa Online-Ressource
|b cr
|2 rdacarrier
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|a Date Completed 14.08.2019
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|a Date Revised 14.08.2019
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|a published: Print-Electronic
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|a Citation Status MEDLINE
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|a Copyright © 2018 Elsevier Inc. All rights reserved.
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|a Calcineurin inhibitors (CNIs) are a cornerstone of the current treatment in solid organ transplantation and autoimmune disease. However, CNIs also bear deleterious effects as they cause glomerular and tubulointerstitial fibrosis in the kidney. We recently identified Y-box protein-1 (YB-1) as a novel downstream effector of CNI-signaling in the cytoplasm of glomerular cells. In the present study, we corroborate the pro-fibrotic role of YB-1 in glomeruli of patients under CNI-treatment. Such effects in glomeruli are significantly mitigated in CNI-treated mice with half-normal YB-1 expression (Yb1+/-). Surprisingly, in the tubulointerstitium we observe an opposite role of the CNI-YB-1 axis. Here, YB-1 is predominantly located to the nuclei and represses transcription of several extracellular matrix genes. Consistently, CNI-treatment in Yb1+/- mice markedly increases pro-fibrotic changes in the tubulointerstitium. In summary, our data provide evidence that fibrotic CNI-induced YB-1 effects in glomerular cells need to be contrasted with beneficial anti-fibrotic effects in the tubulointerstitium
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|a Journal Article
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|a Research Support, Non-U.S. Gov't
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|a CNI-induced nephropathy
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|a Calcineurin inhibitor
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|a Renal fibrosis
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|a Subcellular shuttling
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|a YB-1
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|a Calcineurin Inhibitors
|2 NLM
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|a Transcription Factors
|2 NLM
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| 650 |
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|a YB-1 protein, mouse
|2 NLM
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| 700 |
1 |
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|a Hermert, Daniela
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Wang, Jialin
|e verfasserin
|4 aut
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| 700 |
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|a M Breitkopf, Daniel
|e verfasserin
|4 aut
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| 700 |
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|a Alidousty, Christina
|e verfasserin
|4 aut
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| 700 |
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|a Neusser, Matthias
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Cohen, Clemens D
|e verfasserin
|4 aut
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| 700 |
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|a Gröne, Elisabeth
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Macheleidt, Iris
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Rauen, Thomas
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Braun, Gerald S
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Floege, Jürgen
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Ostendorf, Tammo
|e verfasserin
|4 aut
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| 700 |
1 |
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|a Raffetseder, Ute
|e verfasserin
|4 aut
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| 773 |
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|i Enthalten in
|t Clinical immunology (Orlando, Fla.)
|d 1999
|g 194(2018) vom: 25. Sept., Seite 67-74
|w (DE-627)NLM098196855
|x 1521-7035
|7 nnns
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| 773 |
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|g volume:194
|g year:2018
|g day:25
|g month:09
|g pages:67-74
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|u http://dx.doi.org/10.1016/j.clim.2018.07.002
|3 Volltext
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|d 194
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