Fig 2: miR-124-1 inhibits tumorigenesis via the p38-Akt-JNK pathwayA, B. The activity of the JNK pathway was evaluated in MHCC-LM3 (A) and Huh7 (B) cells transfected with si-CASC3. The activity of the JNK pathway in HCC cells infected with a control lentiviral vector or an miR-124-1expression lentiviral vector was assessed after transduction with a lentiviral vector encoding CASC3 (open reading frame without the 3'-UTR).

Fig 3: Model showing the role of iRhom2 as a positive regulator of PM2.5-induced renal injury. iRhom2 played an essential role in regulating the progression of renal injury in PM2.5-exposed mice, most likely through activating TACE/TNFRs and I?Ba/NF-?B signaling pathways to promote inflammation. In addition, iRhom2 inactivated HO-1/Nrf-2 pathway, whereas activated JNK expression to enhance oxidative stress, thus exacerbating renal injury.

Fig 4: Effects of a recombinant secreted protein acidic and rich in cysteine (rSPARC) and an integrin aVß3 inhibitor at 24 h after modeling. (a) rSPARC exacerbates modified Garcia's score and inhibition of integrin aVß3 suppresses the effects of rSPARC after SAH (n = 6 per group). *P < 0.05 and **P < 0.01. (b) Representative Western blot images and densitometric quantification of expression of phosphorylated p46 and p54 c-Jun N-terminal kinase (p-JNK), phosphorylated p38 (p-p38), interleukin (IL)-6, pro and active matrix metalloproteinase (MMP)-9, ZO-1, and vascular endothelial- (VE-) cadherin. Representative Western blots come from the same samples but multiple membranes. Expression levels of each protein are assessed using ß-actin as an internal control: the levels are expressed as the target protein/ß-actin, p-p38/p38, or p-JNK/JNK and as a ratio of the average level of the sham + PBS group for normalization, because the levels of p38 and JNK are unchanged among the groups (mean ± standard deviation; n = 6 per group). *P < 0.05 and **P < 0.01 vs. sham + phosphate-buffered saline (PBS), †P < 0.05 and ‡P < 0.01 vs. Sham + rSPARC, §P < 0.05 and ¶P < 0.01 vs. SAH + PBS, #P < 0.05 and ##P < 0.01 vs. SAH + rSPARC. cRGD: cyclo(-RGDfK): integrin aVß3 inhibitor.

Fig 5: Models showing that iRhom2 is a positive regulator of alcohol-induced liver fibrosis; iRhom2 plays an important role in regulating the progression of liver fibrosis in alcohol-exposed mice, most likely by activating the TACE/TNFRs/NF-?B signaling pathway to promote inflammation. In addition, iRhom2 exacerbates liver fibrotic lesions by activating JNK expression to enhance oxidative stress via the Nrf2/HO-1 pathway.