IL-22 inhibits ox-LDL-induced apoptosis and increases Bcl-2 expression in CRL-1730 cells
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Supported by National Natural Science Foundation of China (30770997, 30972730, 81072479) and Project of Science and Technology Committee of Shanghai Municipality (09JC1405400, 08QH14001).

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    Abstract:

    ObjectiveTo investigate the effect of interleukin-22 (IL-22) on apoptosis of CRL-1730 cells(human umbilical vein endothelial cell line) induced by ox-LDL and the possible mechanism. MethodsExpression of IL-22 receptor R1 (IL-22R1) mRNA in CRL-1730 cells stimulated with ox-LDL (100 μg/ml) was detected by fluorescence quantitative RT-PCR. Flow cytometry was applied to examine the effect of exogenous IL-22 (20 ng/ml) on the ox-LDL-induced apoptosis of CRL-1730 cells. The expression of Bcl-2, Bcl-xl, Bcl-w, caspase 3, and STAT3 mRNA in CRL-1730 cells treated or untreated with IL-22 and ox-LDL were measured by fluorescence quantitative RT-PCR; the phosphorylation status of STAT3 and the Bcl-2 protein level were examined by Western blotting analysis. ResultsThe expression of IL-22R1 mRNA increased in a time-dependent manner (P<0.05) and peaked at 12 h after ox-LDL stimulation. Treatment with IL-22 significantly inhibited the apoptosis of CRL-1730 cells induced by ox-LDL(P<0.01), increased the expression of anti-apoptosis genes Bcl-2, Bcl-xl, and Bcl-w, and decreased expression of caspase 3 mRNA(P<0.01). STAT3 phosphorylation occurred 1-2 h after IL-22 treatment and Bcl-2 protein expression increased 4 h after IL-22 treatment in ox-LDL stimulated CRL-1730 cells. ConclusionIL-22 can inhibit the pro-apoptosis effect of ox-LDL in the CRL-1730 cells, which might be associated with the increased expression of Bcl-2, Bcl-xl, and Bcl-w mRNA, decreased expression of caspase 3, and induced STAT3 phosphorylation.

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History
  • Received:December 31,2010
  • Revised:January 20,2011
  • Adopted:February 15,2011
  • Online: March 17,2011
  • Published:
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