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. 2016 Mar 1;6:22487. doi: 10.1038/srep22487

Figure 7. siRNA-mediated knockdown of JNK and IRE1 inhibited JFH1 HCV-activated ER stress, NFκB and TGF-β1 luciferase activity.

Figure 7

Huh7.5.1 cells and Huh7.5.1 infected with JFH1 for 3 days were transfected with 25 nM small interfering RNA (siRNA) against JNK, IRE1, ATF6 or PERK. After 48 hours of transfection, cells were transfected with pARE, pERSE, pNFκB or pSMAD-luciferase reporter. ARE-mediated Nrf2, ERSE, pNFκB or pSMAD signaling were monitored by a dual luciferase reporter assay system at 24 hours after luciferase reporter transfection. We found that ARE-mediated Nrf2 signaling was not blocked by JNK, IRE1, ATF6 or PERK-specific knockdown (Fig. 7A). ERSE luciferase signaling was blocked by JNK siRNA (Fig. 7B). The siRNA-mediated knockdown JNK and IRE1 inhibited HCV-activated NFκB and SMAD luciferase activity in JFH1 cells compared to uninfected Huh7.5.1 cells (Fig. 7C,D). *p < 0.05 for comparison of indicated siRNA-mediated knockdown and JFH1-infected cells.