Osteopontin mediating cyclosporine A induced epithelial-to-mesenchymal transition on rat renal tubular epithelial cells

Authors

  • Dongliang Xu,

    Corresponding author
    1. Department of Urology, The First People's Hospital Affiliated to Shanghai Jiao Tong University, Shanghai First People's Hospital, Shanghai, China
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    • Dongliang Xu, Xia Chen and Zhonglei Deng contributed equally to this work.
  • Xia Chen,

    1. Department of Gerontology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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    • Dongliang Xu, Xia Chen and Zhonglei Deng contributed equally to this work.
  • Zhonglei Deng,

    1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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    • Dongliang Xu, Xia Chen and Zhonglei Deng contributed equally to this work.
  • Ruoyun Tan,

    1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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  • Chao Liu,

    1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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  • Pei Lu,

    1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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  • Wei Zhang,

    1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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  • Min Gu

    1. Department of Urology, The First Affiliated Hospital of Nanjing Medical University, Nanjing, Jiangsu Province, China
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Abstract

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.

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