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Article

Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin

  • Authors:
    • Jian Hao
    • Xin Zhao
    • Weimin Yu
    • Xiaoguang Huang
    • Yirong Huang
  • View Affiliations / Copyright

    Affiliations: Department of Nephrology, Shanxi Dayi Hospital, Taiyuan, Shanxi 030032, P.R. China, Department of Radiotherapy, The Second Hospital of Shanxi Medical University, Taiyuan, Shanxi 030001, P.R. China
  • Pages: 459-464
    |
    Published online on: November 2, 2018
       https://doi.org/10.3892/etm.2018.6919
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Abstract

Renal fibrosis is a significant characteristic of chronic kidney diseases. Surfactant protein A (SP‑A) is a recently identified fibrosis‑associated factor in lung fibrosis; however, whether SP‑A has the same role in renal fibrosis has remained elusive. The aim of the present study was to investigate the role of SP‑A and its receptor calreticulin (CRT) in the pathogenesis of kidney fibrosis. The HK‑2 human tubular epithelial cell line was cultured and treated with SP‑A and SP‑A + anti‑CRT. The production of reactive oxygen species (ROS) at 30, 60 and 120 min was examined. Furthermore, cell apoptosis was assessed using an Annexin V assay and the expression of various proteins was measured using western blot analysis. In addition, the cell culture supernatants were collected and the expression of type I collagen was examined using ELISA. Compared with the control group, SP‑A treatment significantly increased the ROS production, type I collagen secretion and cell apoptosis, which was partially inhibited by addition of anti‑CRT. Furthermore, downregulation of matrix metalloproteinase (MMP)2 and ‑9 as well as upregulation of tissue inhibitor of metalloproteinase 1 indicated that SP‑A treatment increased the degree of fibrosis in HK‑2 cells, while addition of anti‑CRT alleviated the fibrotic conditions. Finally, SP‑A treatment significantly increased the expression of phosphorylated (p)‑p38, p‑p‑65 and NADPH oxidase 2, which was partially inhibited by addition of anti‑CRT. In conclusion, SP‑A may participate in the pathogenesis of kidney fibrosis through binding to CRT and activate the mitogen‑activated protein kinase/nuclear factor‑κB‑associated oxidative stress signaling pathway.
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Copy and paste a formatted citation
Spandidos Publications style
Hao J, Zhao X, Yu W, Huang X and Huang Y: Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin. Exp Ther Med 17: 459-464, 2019.
APA
Hao, J., Zhao, X., Yu, W., Huang, X., & Huang, Y. (2019). Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin. Experimental and Therapeutic Medicine, 17, 459-464. https://doi.org/10.3892/etm.2018.6919
MLA
Hao, J., Zhao, X., Yu, W., Huang, X., Huang, Y."Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin". Experimental and Therapeutic Medicine 17.1 (2019): 459-464.
Chicago
Hao, J., Zhao, X., Yu, W., Huang, X., Huang, Y."Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin". Experimental and Therapeutic Medicine 17, no. 1 (2019): 459-464. https://doi.org/10.3892/etm.2018.6919
Copy and paste a formatted citation
x
Spandidos Publications style
Hao J, Zhao X, Yu W, Huang X and Huang Y: Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin. Exp Ther Med 17: 459-464, 2019.
APA
Hao, J., Zhao, X., Yu, W., Huang, X., & Huang, Y. (2019). Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin. Experimental and Therapeutic Medicine, 17, 459-464. https://doi.org/10.3892/etm.2018.6919
MLA
Hao, J., Zhao, X., Yu, W., Huang, X., Huang, Y."Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin". Experimental and Therapeutic Medicine 17.1 (2019): 459-464.
Chicago
Hao, J., Zhao, X., Yu, W., Huang, X., Huang, Y."Surfactant protein A induces the pathogenesis of renal fibrosis through binding to calreticulin". Experimental and Therapeutic Medicine 17, no. 1 (2019): 459-464. https://doi.org/10.3892/etm.2018.6919
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