Β-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. Issue 1 (31st December 2021)

• Record Type: Journal Article
• Authors: Fan, Wenqing; Yuan, Weifeng; Ding, Xiuyan; Zhu, Liqian
• Is Part Of: Virulence. Volume 12:Issue 1(2021)
• Page Start: 1345
• Page End: 1361
• Publication Date: 2021-12-31
• Subjects: BoHV-1 -- HMGB1 -- β-catenin -- mitochondria; Virulence (Microbiology) -- Periodicals; Bacterial diseases -- Periodicals; Molecular microbiology -- Periodicals; 579.05
• DOI: 10.1080/21505594.2021.1926409
• Languages: English
• ISSNs: 2150-5608

Abstract

ABSTRACT: 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, β-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 β-catenin signaling may regulate inflammatory response via affecting HMGB1 signaling.