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The Korean Association of Immunobiologists (대한면역학회)
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Calcium/Calmodulin-Dependent Protein Kinase is Involved in the Release of High Mobility Group Box 1 Via the Interferon-${\beta}$ Signaling Pathway

  • Ma, Lijuan (Department of Pathology, Hallym University College of Medicine) ;
  • Kim, Seon-Ju (Department of Pathology, Hallym University College of Medicine) ;
  • Oh, Kwon-Ik (Department of Pathology, Hallym University College of Medicine)
  • Received : 2012.07.07
  • Accepted : 2012.08.02
  • Published : 2012.08.30
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Abstract

Previously, we have reported that high mobility group box 1 (HMGB1), a proinflammatory mediator in sepsis, is released via the IFN-${\beta}$-mediated JAK/STAT pathway. However, detailed mechanisms are still unclear. In this study, we dissected upstream signaling pathways of HMGB1 release using various molecular biology methods. Here, we found that calcium/calmodulin-dependent protein kinase (CaM kinase, CaMK) is involved in HMGB1 release by regulating IFN-${\beta}$ production. CaMK inhibitor, STO609, treatment inhibits LPS-induced IFN-${\beta}$ production, which is correlated with the phosphorylation of interferon regulatory factor 3 (IRF3). Additionally, we show that CaMK-I plays a major role in IFN-${\beta}$ production although other CaMK members also seem to contribute to this event. Furthermore, the CaMK inhibitor treatment reduced IFN-${\beta}$ production in a murine endotoxemia. Our results suggest CaMKs contribute to HMGB1 release by enhancing IFN-${\beta}$ production in sepsis.

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References

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