Abstract: SA-PO345
Inhibition of NF-κB Signaling in Neural Crest-Derived Fibroblasts Attenuates Renal Fibrosis
Session Information
- Mechanisms Associated with Kidney Fibrosis - II
November 04, 2017 | Location: Hall H, Morial Convention Center
Abstract Time: 10:00 AM - 10:00 AM
Category: Chronic Kidney Disease (Non-Dialysis)
- 308 CKD: Mechanisms of Tubulointerstitial Fibrosis
Authors
- 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
Background
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.
Methods
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.
Results
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.
Conclusion
Results suggest that the NF-κB signaling in fibroblasts originated from neural crest plays an important role in renal fibrosis in chronic kidney disease.
Funding
- Private Foundation Support