Bcl-3 is a novel biomarker of renal fibrosis in chronic kidney disease
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Ran Chen1,*, Lunshan Wang2,*, Sanhong Liu3, Xi Chen1, Yiming Hu1, Hanshao Liu1, Haohao Zhang1, Yuhang Jiang1, Qi Wang1, Deji Ye1, Lingling Li1, Dandan Liu1, Xiaorong Pan4, Lixin Wei4, Xuemei Li5 and Xiaoren Zhang1
1Key Laboratory of Stem Cell Biology, Institute of Health Sciences, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai Jiao Tong University School of Medicine, Shanghai 200031, China
2Clinical Laboratory Department, The Chinese People’s Liberation Army 105th Hospital, Hefei 230001, China
3Shanghai Institute for Advanced Immunochemical Studies, ShanghaiTech University, Shanghai 201210, China
4Tumor Immunology and Gene Therapy Center, Eastern Hepatobiliary Surgery Hospital, The Second Military Medical University, Shanghai 200433, China
5Department of Nephrology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, Beijing 100723, China
*These authors have contributed equally to this work
Xiaoren Zhang, email: firstname.lastname@example.org
Xuemei Li, email: email@example.com
Keywords: Bcl-3, renal fibrosis, chronic kidney disease, unilateral ureteral obstruction, biomarker
Received: June 27, 2017 Accepted: August 31, 2017 Published: October 09, 2017
Progressive renal fibrosis in chronic kidney disease (CKD) greatly contributes to end-stage renal failure and is associated with high mortality. The identification of renal fibrosis biomarkers for the diagnosis and the monitoring of disease progression in CKD is urgently needed. Whole-transcriptomic analysis of renal tissues in a unilateral ureteral obstruction (UUO) mouse model revealed that the mRNA level of Bcl-3, an atypical member of the IκB family, was induced 6.3-fold 2 days after UUO. Compared with renal tissues in sham-operated mice, increases in Bcl-3 mRNA and protein in the renal tissues in the UUO model were accompanied with increases in other markers of renal fibrosis, including human epididymis protein 4 (HE4), a recently identified biomarker of renal fibrosis. Immunohistochemical analysis revealed that both Bcl-3 and HE4 were located in the plasma of renal tubule cells. Serum protein levels of Bcl-3 and HE4 rose with the development of renal fibrosis in UUO mouse model. We found that the serum protein levels of both HE4 and Bcl-3 were elevated in CKD patients compared with healthy controls. Moreover, a significant positive correlation between Bcl-3 and HE4 (r = 0.939, p < 0.0001) was observed in CKD patients. These data suggest that Bcl-3 can serve as a novel valuable biomarker of renal fibrosis in CKD.
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