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Dexamethasone Induces $Fc{\gamma}RIIb$ Expression in RBL-2H3 Cells

  • Silwal, Prashanta (Research Institute for Medical Sciences and Department of Biochemistry, College of Medicine, Chungnam National University) ;
  • Lee, Mi-Nam (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Lee, Choong-Jae (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • Hong, Jang-Hee (Department of Pharmacology, College of Medicine, Chungnam National University) ;
  • NamGung, Uk (Department of Oriental Medicine, Daejeon University) ;
  • Lee, Zee-Won (Division of Life Science, Korea Basic Science Institute) ;
  • Kim, Jinhyun (Department of Internal Medicine, Chungnam National University Hospital) ;
  • Lim, Kyu (Research Institute for Medical Sciences and Department of Biochemistry, College of Medicine, Chungnam National University) ;
  • Kweon, Gi Ryang (Research Institute for Medical Sciences and Department of Biochemistry, College of Medicine, Chungnam National University) ;
  • Park, Jong Il (Research Institute for Medical Sciences and Department of Biochemistry, College of Medicine, Chungnam National University) ;
  • Park, Seung Kiel (Research Institute for Medical Sciences and Department of Biochemistry, College of Medicine, Chungnam National University)
  • Received : 2012.07.04
  • Accepted : 2012.11.10
  • Published : 2012.12.31

Abstract

Mast cells are involved in allergic responses, protection against pathogens and autoimmune diseases. Dexamethasone (Dex) and other glucocorticoids suppress $Fc{\varepsilon}RI$-mediated release of inflammatory mediators from mast cells. The inhibition mechanisms were mainly investigated on the downstream signaling of Fc receptor activations. Here, we addressed the effects of Dex on Fc receptor expressions in rat mast cell line RBL-2H3. We measured mRNA levels of Fc receptors by real-time PCR. As expected, Dex decreased the mRNA levels of activating Fc receptor for IgE ($Fc{\varepsilon}R$) I and increased the mRNA levels of the inhibitory Fc receptor for IgG $Fc{\gamma}RIIb$. Interestingly, Dex stimulated transcriptions of other activating receptors such as Fc receptors for IgG ($Fc{\gamma}R$) I and $Fc{\gamma}RIII$. To investigate the mechanisms underlying transcriptional regulation, we employed a transcription inhibitor actinomycin D and a translation inhibitor cycloheximide. The inhibition of protein synthesis without Dex treatment enhanced $Fc{\gamma}RI$ and $Fc{\gamma}RIII$ mRNA levels potently, while $Fc{\varepsilon}RI$ and $Fc{\gamma}RIIb$ were minimally affected. Next, we examined expressions of the Fc receptors on cell surfaces by the flow cytometric method. Only $Fc{\gamma}RIIb$ protein expression was significantly enhanced by Dex treatment, while $Fc{\gamma}RI$, $Fc{\gamma}RIII$ and $Fc{\varepsilon}RI$ expression levels were marginally changed. Our data showed, for the first time, that Dex regulates Fc receptor expressions resulting in augmentation of the inhibitory receptor $Fc{\gamma}RIIb$.

Keywords

References

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