Beta-Catenin Has Potential Effects On The Expression, Subcellular Localization, And Release Of High Mobility Group Box 1 During Bovine Herpesvirus 1 Productive Infection In Mdbk Cell Culture

High mobility group box 1 (HMGB1), a ubiquitous DNA-binding protein, can be released into extracellular space and function as a strong proinflammatory cytokine, which plays critical roles in the pathogenesis of various inflammatory diseases. Here, we showed that BoHV-1 productive infection in MDBK cells at later stage significantly increases HMGB1 mRNA expression and the protein release, but decreases the steady-state protein levels. Virus infection increases accumulation of HMGB1 protein in both nucleus and mitochondria, and relocalizes nuclear HMGB1 to assemble in highlighted foci via a confocal microscope assay. Interestingly, beta-catenin-specific inhibitor iCRT14 is able to increase HMGB1 transcription and the protein release, and subcellular translocation in virus-infected cells. HMGB1-specific inhibitor, glycyrrhizin, could differentially affect virus gene transcription such as, the viral regulatory protein bICP0, bICP4 and bICP22, as well as glycoprotein gD. In summary, our data provides a novel mechanism that beta-catenin signaling may regulate inflammatory response via affecting HMGB1 signaling.