Regulation of Heat Shock Protein 27 on the Proliferation of Vesicular Stomatitis Virus in vitro
This study was conducted to investigate the effect and mechanism of heat shock protein 27(HSP27)on the proliferation of vesicular stomatitis virus(VSV)in vitro and the retinoid acid-inducible gene-Ⅰ-like receptor(RLR)signaling pathway mediated by VSV infection.Real-time quantitative PCR,Western blotting,Co-immunoprecipitation,TCID50 assay,and immuno-fluorescence methods were employed to reveal the effects of VSV infection on the mRNA and protein expression of HSP27,and then the effects of overexpression and interference with HSP27 on the proliferation of VSV,and further explore the effects of HSP27 on the RLR signaling path-way mediated by VSV infection.Finally,the interaction and co-localization between HSP27 and the target molecules in RLR signaling pathway were analyzed.The results showed that VSV in-fection could increase the gene transcription and protein expression of HSP27,both stable and transient overexpression of HSP27 significantly inhibited the proliferation of VSV in vitro.Inter-fering with HSP27 expression in host cells promoted the proliferation of VSV.Further studies showed that HSP27 enhanced both VSV and retinoic acid-inducible gene Ⅰ protein(RIG-Ⅰ)media-ted IFN-β production and the protein expression of RIG-Ⅰ,and that HSP27 interacted with RIG-Ⅰand co-localized in the cytoplasm.This study for the revealed the molecular mechanism by which HSP27 targets RIG-Ⅰ to upregulate its expression,enhance the transduction of RLR signaling pathways,and then negatively regulate the proliferation of VSV in vitro,laying a foundation for further revealing the mechanism of host factor HSP27 in viral infection.
heat shock protein 27vesicular stomatitis virusRLR signaling pathwayRIG-Ⅰ
万方数据
维普
