Literature DB >> 25682062

C3a and C5a receptor antagonists ameliorate endothelial-myofibroblast transition via the Wnt/β-catenin signaling pathway in diabetic kidney disease.

Ling Li1, Lijia Chen1, Jing Zang1, Xi Tang1, Yan Liu2, Jie Zhang3, Lin Bai3, Qinghua Yin1, Yanrong Lu3, Jingqiu Cheng3, Ping Fu1, Fang Liu4.   

Abstract

BACKGROUND: Endothelial-myofibroblast transition (EndMT) has been implicated in the pathogenesis of diabetic renal fibrosis. In this study, the effect of the complement fragments C3a/C5a and their receptor antagonists C3aRA and C5aRA on EndMT in diabetic kidney disease (DKD) and the possible mechanisms were investigated.
METHODS: The coexpression of CD31 with α-smooth muscle (α-SMA), C3a receptor (C3aR) and C5a receptor (C5aR) was detected in human renal biopsy tissue obtained from patients with early and advanced DKD and in normal renal tissues from patients with renal-cell carcinoma. The effects of C3aRA and C5aRA on EndMT and the expression of C3a/C3aR, C5a/C5aR, α-SMA, CD31, TGFβ, FN and β-catenin were examined in a streptozotocin (STZ)-induced rat model of DKD and in human renal glomerular endothelial cells (HRGECs) cultured in high glucose and with C3a/C5a, and DKK1 (a Wnt/β-catenin inhibitor).
RESULTS: Double-labeling of α-SMA, C3aR, C5aR and CD31 was detected in the glomerulus of renal tissues obtained from biopsies of patients with DKD. Upregulated expression of α-SMA, TGF-β, FN and β-catenin and downregulated expression of CD31 were detected in the GECs of diabetic rats. The expression of these proteins was inhibited by treatment with C3aRA/C5aRA. In vitro, C3aRA/C5aRA and DKK1 ameliorated the high glucose-induced EndMT and the subsequent expression of α-SMA, TGFβ, FN and β-catenin in HRGECs.
CONCLUSIONS: The blockade of C3aR/C5aR and the downstream Wnt/β-catenin pathway may prevent EndMT and alleviate fibrosis in the glomeruli of individuals with DKD.
Copyright © 2015 Elsevier Inc. All rights reserved.

Entities:  

Keywords:  C3a receptor antagonists; C5a receptor antagonists; Diabetic kidney disease; Endothelial-myofibroblast transition; Wnt/β-catenin signaling pathway

Mesh:

Substances:

Year:  2015        PMID: 25682062     DOI: 10.1016/j.metabol.2015.01.014

Source DB:  PubMed          Journal:  Metabolism        ISSN: 0026-0495            Impact factor:   8.694


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