SDF‑1/CXCR4 induces epithelial‑mesenchymal transition through activation of the Wnt/β‑catenin signaling pathway in rat chronic allograft nephropathy

摘要: Epithelial-mesenchymal transition (EMT) has been demonstrated to serve a crucial role in the progression of interstitial fibrosis, which is one principal pathological features chronic allograft nephropathy (CAN). However, best our knowledge, mechanisms EMT CAN have not investigated. In present study, effect stromal cell-derived factor 1 (SDF-1) and Wnt signaling pathway on following kidney transplantation was The model established using Fisher 344 Lewis rats, treated with low-dose cyclosporine or without AMD3100. confirmed by alterations damage index scoring, western blotting reverse transcription-quantitative polymerase chain reaction. AMD3100 group, there were lower expression levels α-SMA higher E-cadherin, indicated that ameliorated tissue analyzed an mRNA + long noncoding (lnc)RNA microarray. A total 506 mRNAs 404 lncRNAs be significantly differentially expressed between two groups, revealed involvement SDF-1/CXC chemokine receptor 4 (CXCR4) pathway. SDF-1 induce vitro through upregulation α-SMA, downregulation E-cadherin wound healing assay, rat renal tubular epithelial cells via nuclear accumulation β-catenin, all inhibited either DKK-1. CXXC finger protein 5 (CXXC5), negative regulator pathway, downregulated treatment SDF-1, but Thus, CXXC5 may downstream SDF-1/CXCR4 EMT. conclusion, induces novel mechanism therapeutic target fibrosis rats.