|
KMID : 0923620120120040148
|
|
Immune Network
2012 Volume.12 No. 4 p.148 ~ p.154
|
|
|
Calcium/Calmodulin-Dependent Protein Kinase is Involved in the Release of High Mobility Group Box 1 Via the Interferon-β Signaling Pathway
|
|
Ma Lijuan
Kim Seon-Ju
Oh Kwon-Ik
|
|
|
Abstract
|
|
|
|
Previously, we have reported that high mobility group box 1 (HMGB1), a proinflammatory mediator in sepsis, is released via the IFN-β-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-β production. CaMK inhibitor, STO609, treatment inhibits LPS-induced IFN-β 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-β production although other CaMK members also seem to contribute to this event. Furthermore, the CaMK inhibitor treatment reduced IFN-β production in a murine endotoxemia. Our results suggest CaMKs contribute to HMGB1 release by enhancing IFN-β production in sepsis.
|
|
|
KEYWORD
|
|
|
Endotoxin shock, Cytokines, Inflammation, Signal transduction
|
|
|
FullTexts / Linksout information
|
|
 
|
|
|
Listed journal information
|
|
   
|
|