Interleukin-20 induced cell death in renal epithelial cells and was associated with acute renal failure

H. H. Li, Y. H. Hsu, C. C. Wei, P. T. Lee, W. C. Chen, M. S. Chang

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22 Citations (Scopus)

Abstract

Acute renal failure is an abrupt decrease in renal function. Interleukin (IL)-10 inhibits ischemic and cisplatin-induced acute renal failure. We aimed to determine whether IL-20 affects renal tubular epithelial cells and is associated with acute renal failure. We analyzed the expression of IL-20 and its receptor (R) in the kidneys of rats with HgCl2-induced acute renal failure. Reverse transcription-PCR showed upregulated IL-20, and its receptors and immunohistochemical staining showed strongly expressed IL-20 protein in proximal tubular epithelial cells. We analyzed human proximal tubular epithelial (HK-2) cells, which expressed both IL-20 and its receptors. IL-20 specifically induced mitochondria-dependent apoptosis by activating caspase 9 in HK-2 cells. IL-20 also activated c-Jun N-terminal kinase and extracellular signal-regulated kinase 1/2, the downstream signals implicated in the apoptosis of HK-2 cells. Furthermore, IL-20 upregulated the transcripts of transforming growth factor (TGF)-β1, a critical mediator of renal injury. In hypoxic HK-2 cells, IL-20 and IL-22R1 transcripts increased, and IL-20 upregulated IL-1β transcripts. In vivo study further demonstrated that anti-IL-20 antibody reduced the expression of TGF-β1 and IL-1β and the number of damaged tubular cells in the kidneys of rats with acute renal failure. We concluded that IL-20 may be involved in the injury of renal epithelial cells in acute renal failure.

Original languageEnglish
Pages (from-to)395-404
Number of pages10
JournalGenes and Immunity
Volume9
Issue number5
DOIs
Publication statusPublished - 2008 Jul 1

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All Science Journal Classification (ASJC) codes

  • Immunology
  • Genetics
  • Genetics(clinical)

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