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Osteopontin mediating cyclosporine A induced epithelial‐to‐mesenchymal transition on rat renal tubular epithelial cells
Author(s) -
Xu Dongliang,
Chen Xia,
Deng Zhonglei,
Tan Ruoyun,
Liu Chao,
Lu Pei,
Zhang Wei,
Gu Min
Publication year - 2014
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1002/cbin.10149
Subject(s) - osteopontin , downregulation and upregulation , epithelial–mesenchymal transition , chemistry , snai1 , microbiology and biotechnology , gene knockdown , fibronectin , cancer research , biology , cell , immunology , biochemistry , apoptosis , gene
Osteopontin (OPN) is highly correlated with cyclosporine A (CsA) nephrotoxicity. As epithelial‐to‐mesenchymal transition (EMT) of renal tubular epithelial cells plays an important role in CsA nephropathy, we investigated whether OPN mediated EMT of renal tubular epithelial cells upon CsA stimulation. OPN knockdown suppresses CsA induced EMT on NRK52E cells, and it also attenuates downregulation of E‐cadherin and upregulation of α‐smooth muscle actin (α‐SMA) and fibronectin (FN) that are induced by CsA. OPN alone can induce EMT on NRK52E cells, which also results in upregulation of TGF‐β1. Thus, OPN is a causative factor in mediating CsA induced EMT on NRK52E cells.