Fig 1: Effect of activated LXR on cholesterol quantity. (A) Activated LXR decreases cholesterol quantity in HCMV infected human foreskin fibroblast. (B) Relative cholesterol levels in virions. (C) The viral titers of cells and virus particles with and without LXR agonist GW3965 treatment have been provided *P < 0.05.
Fig 2: Reverse regulation of ß-catenin reversed the effect of YB-1 on lipid synthesis in LO2 cells. (A) Oil Red O staining showing lipid deposits in each group (scale bar =100 µm, n =3 per group); (B,C) the expression levels of SREBP-1c, LXRa, FXR1, and PPARa (*, P<0.05 compared with groups without any treatment, n=3 per experiment); (D) RT-PCR indicating the gene expression of SREBP-1c, LXRa, FXR1, and PPARa (*, P<0.05 compared with groups without any treatment, n=3 per experiment); (E,F) ELISA assay detected the contents of TNFa and IL-6 in the supernatants of the above groups (*, P<0.05 compared with groups without any treatment, n=3 per experiment). YB-1, y-box binding protein 1; qRT-PCR, Quantitative Real-time PCR; ELISA, Enzyme-linked immunosorbent assay; SREBP-1c, sterol regulatory element binding protein-1c; LXRa, Liver X Receptor a; FXR1, farnesoid X receptor1; PPARa, peroxisome proliferator-activated receptor-alpha; TNFa, tumor necrosis factor a, IL-6, interleukin 6.
Fig 3: Knockdown of AMPKa1 abolishes CTRP9 protective effects in VSMCs VSMC cells were transfected with an siRNA targeting AMPa1 (siRNAa1), a control siRNA (NC), or were not transfected (-). Cells were then treated with 5 µg/ml cholesterol in the presence of CTRP9 (10 µg/ml) for 72 hrs. (A) Representative Western blot of ACTA2, phospho-AMPK (p-AMPK), total AMPK (AMPK), TLR4, MyD88, phospho-p65 (p-p65), total p65 (t-p65), LOX-1, LXR, ABCA1, ABCG1, ICAM-1 and VCAM-1 in VSMCs from each treatment. (B–L) Quantification of Western blot images. Values represent the means ± S.D. of triplicate reactions and are representative of three independent experiments. *P < 0.05, **P < 0.01, ***P < 0.001, ****P < 0.0001.
Fig 4: PARP-1 inhibits LXR-induced ABCA1 transcription in INS-1 cells. (A) Confirmation of the interaction between LXR and PARP-1 in INS-1 cells using coimmunoprecipitation (Co-IP) assay. (B) LXRa poly(ADP-ribosyl)ation was detected in INS-1 by Poly(ADP-ribosyl)ation Assay. (C,D) INS-1 cells were transfected with si-PARP-1 in the presence or absence of LXR receptor agonist T0901317 and examined for the mRNA expression and protein levels of ABCA1 by real-time PCR and immunoblotting. n = 3 for each experiment. **P < 0.01 compared with the si-NC + DMSO group, #P < 0.05 compared with the si-NC + T0901317 group.
Fig 5: Effects of activated LXR on virion maturation in the cytoplasm of infected cells. NIEP, virions, and abnormal virions can be found in panels (A,B). The hollow diamond-head arrow points to the non-infectious enveloped particle. The solid arrow indicates the infectious virion. The hollow arrow shows the abnormal virion containing the viral genome but no intact bilayer membrane structure at a magnification of 40,000. The numbers and the percentages of each type of virions in VAC of infected cells treated with or without GW3965 are presented in panels (C,D), respectively. Data were analyzed by the t-test *P < 0.05.
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