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October-2015 Volume 10 Issue 4

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Article

Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome

  • Authors:
    • Yumei Liang
    • Yinyin Chen
    • Ying Chen
    • Yuting Gong
  • View Affiliations / Copyright

    Affiliations: Department of Nephrology, Hunan Provincial People's Hospital, First Affiliated Hospital of Hunan Normal University, Changsha, Hunan 410005, P.R. China
  • Pages: 1556-1562
    |
    Published online on: July 30, 2015
       https://doi.org/10.3892/etm.2015.2665
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Abstract

The present study aimed to investigate the changes in the expression levels of the glucocorticoid receptor (GR) and its subtypes in patients with recurrent renal syndrome. In addition, the effects of tumour necrosis factor α (TNF‑α) and a TNF‑α monoclonal antibody on these receptors in peripheral blood mononuclear cells (PBMCs) isolated from the patients was analysed. Furthermore, a new treatment method for recurrent renal syndrome was explored. The serum levels of TNF‑α in the normal (A), stable renal syndrome (B) and renal syndrome recurrence (C) groups of patients were determined by enzyme‑linked immunosorbent assay (ELISA). The mRNA and protein expression levels of GR, GRα and GRβ were determined by ELISA, western blot analysis and quantitative polymerase chain reaction in PBMC cultures from the three groups in the absence of intervention (blank control) and following stimulation with methylprednisolone, TNF‑α and/or TNF‑α monoclonal antibody. Group C exhibited higher expression levels of TNF‑α and GRβ but a lower level of GRα expression (P<0.05) compared with the other groups. Regardless of methylprednisolone intervention, the expression levels of GR and GRβ in the three groups following stimulation by TNF‑α were significantly higher compared with those in the respective blank control, whereas in group C, the GRα expression levels following TNF‑α treatment were lower compared with those in the control group (P<0.05). The treatment of group C with TNF‑α monoclonal antibodies resulted in higher GRα expression but lower GRβ expression compared with those in the blank control (P<0.05). The change in the ratios of the GR subtypes may be associated with renal syndrome recurrence. TNF‑α may be involved in renal syndrome relapse by changing the levels of GR as well as the proportion of the GR subtypes. TNF-α monoclonal antibodies may mitigate the changes in the ratios of these subtypes.
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Copy and paste a formatted citation
Spandidos Publications style
Liang Y, Chen Y, Chen Y and Gong Y: Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome. Exp Ther Med 10: 1556-1562, 2015.
APA
Liang, Y., Chen, Y., Chen, Y., & Gong, Y. (2015). Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome. Experimental and Therapeutic Medicine, 10, 1556-1562. https://doi.org/10.3892/etm.2015.2665
MLA
Liang, Y., Chen, Y., Chen, Y., Gong, Y."Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome". Experimental and Therapeutic Medicine 10.4 (2015): 1556-1562.
Chicago
Liang, Y., Chen, Y., Chen, Y., Gong, Y."Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome". Experimental and Therapeutic Medicine 10, no. 4 (2015): 1556-1562. https://doi.org/10.3892/etm.2015.2665
Copy and paste a formatted citation
x
Spandidos Publications style
Liang Y, Chen Y, Chen Y and Gong Y: Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome. Exp Ther Med 10: 1556-1562, 2015.
APA
Liang, Y., Chen, Y., Chen, Y., & Gong, Y. (2015). Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome. Experimental and Therapeutic Medicine, 10, 1556-1562. https://doi.org/10.3892/etm.2015.2665
MLA
Liang, Y., Chen, Y., Chen, Y., Gong, Y."Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome". Experimental and Therapeutic Medicine 10.4 (2015): 1556-1562.
Chicago
Liang, Y., Chen, Y., Chen, Y., Gong, Y."Role of the glucocorticoid receptor in the recurrence of primary nephrotic syndrome". Experimental and Therapeutic Medicine 10, no. 4 (2015): 1556-1562. https://doi.org/10.3892/etm.2015.2665
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