Department of Urology, The First People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai First People's Hospital, 100 Haining Road, Shanghai, 200080, China.
Cell Biol Int. 2014 Jan;38(1):8-15. doi: 10.1002/cbin.10149. Epub 2013 Nov 7.
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.
骨桥蛋白（OPN）与环孢素 A（CsA）肾毒性高度相关。由于肾小管上皮细胞的上皮-间充质转化（EMT）在 CsA 肾病中起重要作用，我们研究了 OPN 是否介导 CsA 刺激下肾小管上皮细胞的 EMT。OPN 敲低抑制了 CsA 诱导的 NRK52E 细胞 EMT，同时也减弱了 CsA 诱导的 E-钙黏蛋白下调和α-平滑肌肌动蛋白（α-SMA）和纤维连接蛋白（FN）的上调。OPN 本身可诱导 NRK52E 细胞发生 EMT，这也导致 TGF-β1 的上调。因此，OPN 是介导 NRK52E 细胞中 CsA 诱导的 EMT 的一个致病因素。
