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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
Immune Network ; : 148-154, 2012.
Article in English | WPRIM | ID: wpr-192565
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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Full text: Available Index: WPRIM (Western Pacific) Main subject: Phosphorylation / Phosphotransferases / Protein Kinases / Benzimidazoles / Signal Transduction / Cytokines / Interferon-beta / Sepsis / Endotoxemia / HMGB1 Protein Language: English Journal: Immune Network Year: 2012 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Phosphorylation / Phosphotransferases / Protein Kinases / Benzimidazoles / Signal Transduction / Cytokines / Interferon-beta / Sepsis / Endotoxemia / HMGB1 Protein Language: English Journal: Immune Network Year: 2012 Type: Article