Journal: International immunopharmacology
Article Title: Activation of cGAS-STING signaling pathway promotes liver fibrosis and hepatic sinusoidal microthrombosis.
doi: 10.1016/j.intimp.2023.111132
Figure Lengend Snippet: Fig. 5. Overexpression of cGAS-STING signaling pathway exacerbates TGF-β1-mediated activation of HSCs. Expression levels of cGAS and STING were detected by WB after transfection with empty-vector , cGAS-overexpression plasmid or STING-overexpression plasmid (A-D). Transfected LX-2 cells were treated with TGF-β1 (20 ng/mL) for 24 h, then subjected to analysis of Col-1α1 and α-SMA expression levels via RT-qPCR and WB (E and F). mRNA expression levels of cGAS, STING, IRF3, TBK1, and inflammatory factors (IL-1β, IL-6, CXCL-1, and IFN-β) in the control group (untreated LX-2 cells), the model group (activated LX-2 cells), the si-cGAS and si-STING group, the cGAS-OE and STING-OE group (G and H). LX-2 cells were transfected with si-cGAS, si-STING, cGAS-OE or STING-OE, and then treated with TGF-β1. The protein expression of Phospho-STING was determined by Western blotting (I and J). *: P < 0.05; **: P < 0.01; ***: P < 0.001 vs. con trol group.
Article Snippet: The primary antibodies were as follows: cGAS (1:1000, CST, USA), STING (1:1000, Abcam, USA), Phospho-STING (1:1000, Abcam, USA), Col-1α1 (1:1000, Proteintech, USA), β-actin (1:5000, Proteintech, USA) and GAPDH (1:5000, Proteintech, USA).
Techniques: Over Expression, Activation Assay, Expressing, Transfection, Plasmid Preparation, Quantitative RT-PCR, Control, Western Blot