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Abstract: SA-PO345

Inhibition of NF-κB Signaling in Neural Crest-Derived Fibroblasts Attenuates Renal Fibrosis

Session Information

Category: Chronic Kidney Disease (Non-Dialysis)

  • 308 CKD: Mechanisms of Tubulointerstitial Fibrosis


  • Yoshida, Tadashi, Keio University School of Medicine, Tokyo, Japan
  • Yamashita, Maho, Keio University School of Medicine, Tokyo, Japan
  • Hayashi, Matsuhiko, Keio University School of Medicine, Tokyo, Japan

It has been recently reported that renal fibroblasts are derived from neural crest and phenotypic conversion of fibroblasts into myofibroblasts contributes to renal fibrosis in chronic kidney disease. The aim of the present study was to determine whether the NF-κB signaling in neural crest-derived fibroblasts was involved in renal fibrosis in a mouse unilateral ureteral obstruction (UUO) model.


Transgenic (P0-Cre/IκBΔN) mice, in which truncated IκB was expressed and the NF-κB signaling was inhibited selectively in neural crest-derived cells, were generated. Renal fibrosis and infiltration of inflammatory cells were examined in P0-Cre/IκBΔN and control mice following UUO.


In response to UUO, renal fibrosis was developed in P0-Cre/IκBΔN and control mice, as determined by Masson trichrome staining and SM α-actin staining. However, of importance, renal fibrosis was significantly attenuated in P0-Cre/IκBΔN mice, as compared to control mice 14 days after UUO. By contrast, renal infiltration of inflammatory cells, including neutrophils, F4/80-positive macrophages, and CD3-positive lymphocytes, was not different between P0-Cre/IκBΔN and control mice.


Results suggest that the NF-κB signaling in fibroblasts originated from neural crest plays an important role in renal fibrosis in chronic kidney disease.


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