Fig. 3: Loss of RHBDL4 in THP-1 cells leads to TMED7 stabilization and consequently to increased TLR4 cell surface level and signaling. | Nature Communications

Fig. 3: Loss of RHBDL4 in THP-1 cells leads to TMED7 stabilization and consequently to increased TLR4 cell surface level and signaling.

From: RHBDL4-triggered downregulation of COPII adaptor protein TMED7 suppresses TLR4-mediated inflammatory signaling

Fig. 3

a TMED7 expression is increased in THP-1 cells transfected with siRNA (si) targeting RHBDL4 (R4) relative to control siRNA (ctrl) as analyzed by western blot (WB) analysis. Actin is used as a loading control. Right panel, TMED7 quantification in siR4-treated cells relative to control (means ± SEM, n = 3; **p < 0.01, two-sided Student’s t test, p = 0.005). b TLR4 cell surface levels are increased in THP-1 cells transfected with siR4 compared to cells treated with sictrl. Cells have been stained with anti-TLR4-PE and analyzed by flow cytometry. Gray curve represents PE-coupled isotypic control (IgG). Representative histogram (left) and MFI ratio (right) of siR4-treated versus sictrl-treated cells. (means ± SEM, n = 4; *p < 0.05, two-sided Student’s t test, p = 0.0244). c THP-1 cells were transfected either with sictrl, siR4, siTMED7 or a combination of the latter two and treated with LPS (1 µg/ml) for 6 h. Normalized transcriptional levels of TNFα and IL-6 relative to LPS-treated cells. Both TNFα (n = 3) and IL-6 (n = 4) expression increases upon knockdown of RHBDL4 that depends on TMED7 expression (means ± SEM; **p < 0.01, two-sided Student’s t test, TNFαː sicon vs. siR4 p = 0.0038; IL-6: sicon vs. siR4 p = 0.0036, sicon vs. siTMED7 p = 0.0012). Source data are provided as a Source Data file.

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