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为探讨Rho B(ras homolog family member B)靶蛋白MYH9(nonmuscle myosin heavy chain IIa)与TRIF-GEFH1-Rho B信号途径的关系,通过实时定量PCR技术、si RNA干扰技术、激光共聚焦显微镜、流式细胞术以及基因敲除小鼠等,分析了MYH9与TRIF(TIR domain-containing adapter inducing IFNβ)途径、GEFH1(guanine nucleotide-exchange factors H1)以及MHCII(major histocompatibility complex II)的关系。结果显示,在LPS(lipopolysaccharide)刺激后,MYH9的m RNA表达在野生型小鼠的树突状细胞(dendritic cells,DCs)中增加,在TRIF基因敲除小鼠的DCs中则未被上调。在野生型小鼠中MYH9的m RNA上调可被GEFH1的si RNA明显抑制(P<0.01)。同时,在LPS刺激后,MYH9与MHCII在细胞内共定位。MYH9的si RNA还抑制了DCs中LPS介导的MHCII在细胞表面的表达(P<0.05)。这些结果表明,MYH9与TRIF-GEFH1-Rho B信号途径存在相关性。
To investigate the relationship between MYH9 (MYH9) and TRIF-GEFH1-Rho B signaling pathway in Rho B gene (Rho B), real-time quantitative PCR, si RNA interference technique, confocal laser scanning microscopy Cytokines and knockout mice, etc. The relationship between MYH9 and TRIF (TIR domain-containing adapter inducing IFNβ) pathway, GEFH1 (guanine nucleotide-exchange factors H1), and MHCII (major histocompatibility complex II) was analyzed. The results showed that MYH9 m RNA expression increased in dendritic cells (DCs) of wild-type mice and not in DCs of TRIF knockout mice after lipopolysaccharide stimulation. Upregulation of MYH9 m RNA in wild-type mice was significantly inhibited by si RNA of GEFH1 (P <0.01). Meanwhile, MYH9 and MHCII co-localized intracellularly after LPS stimulation. SiRNA of MYH9 also inhibited LPS-mediated MHC II expression on the cell surface in DCs (P <0.05). These results indicate that there is a correlation between MYH9 and the TRIF-GEFH1-Rho B signaling pathway.