Fig. 5: Lsd1 directly regulates Tlr4 expression in hepatitis B virus (HBV)-infected HK-2 cells. | Cell Death & Disease

Fig. 5: Lsd1 directly regulates Tlr4 expression in hepatitis B virus (HBV)-infected HK-2 cells.

From: The histone demethylase LSD1 promotes renal inflammation by mediating TLR4 signaling in hepatitis B virus-associated glomerulonephritis

Fig. 5

a Western blot analysis of H3K4 and H3K9 methylation in HK-2 cells co-transfected with pCMV-HBV1.3 and shCtrl or shLSD1-2 for 48 h. b, d, e Chromatin immunoprecipitation-quantitative PCR analysis of LSD1 (b), H3K9me1/2 (d), and H3K4me1/2 (e) enrichment in the Tlr4 promoter regions. Signals are shown as a percentage of the input. IgG immunoglobulin G. c Luciferase activity in lysates of HK-2 cells transfected with luciferase reporter plasmids of pGL3-basic vector (vector), toll-like receptor 4 (TLR4) promoter (pTLR4-wt), or TLR4 promoter with mutation on the predicted LSD1-binding site (pTLR4-mut). Relative luciferase activity for each group was standardized using the value from the control cells transfected with pGL3-basic vector. f Western blot analysis of TLR4 in HBV-infected HK-2 cells transfected with shCtrl or shLSD1-2 for 48 h. g Western blot analysis of TLR4 in HBV-infected HK-2 cells treated with saline (Ctrl) or tranylcypromine (TCP, 10 µM) for 12 h. Data are presented as the mean ± SD (N = 3). *P < 0.05 versus shCtrl; #P < 0.05 versus HBV + shCtrl group; †P < 0.05 versus Ctrl. n.s. not significant

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