Fig. 3
From: Mitochondrial DNA leakage induces odontoblast inflammation via the cGAS-STING pathway
The cGAS-STING pathway regulated LPS-induced mDPC6T inflammation. a–b mDPC6T cells were transfected with anti-cGAS siRNA (a) or anti-STING siRNA (b) twice at an interval of 48 h. LPS (20 μg/ml) was administered 24 h after the second transfection. The phosphorylation of TBK1 was analyzed by western blotting. The quantitative data represent the relative ratio of the target protein to total TBK1. c–d Real-time PCR was performed to detect the expression of IL-6, CXCL10, IFN-α and IFN-β in mDPC6T cells in response to 24 h of LPS stimulation without or with cGAS (c) or STING (d) knockdown. GAPDH served as the loading control. e Western blotting was performed to analyze the cytoplasmic and nuclear protein levels of p65 and IRF3 in STING-knockdown mDPC6T cells. β-tubulin served as the loading control for cytoplasmic proteins. Lamin A/C served as the loading control for nuclear proteins. The data are the mean ± SEM, n = 3 (*p < 0.05, **p < 0.01 ***p < 0.001)