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Fig. 5 | Arthritis Research & Therapy

Fig. 5

From: Mitochondrial protein CMPK2 regulates IFN alpha-enhanced foam cell formation, potentially contributing to premature atherosclerosis in SLE

Fig. 5

Effect of CMPK2 knockout on TDMs. The CMPK2 gene was knocked out through the CRISPR/Cas9 approach in THP-1 cells, as explained in detail in the “Materials and methods” section, and two clones, #3-2 and #3-8, were obtained; their partial sequences are shown (a). The expression of CMPK2 induced by IFN-α was completely abolished in CMPK2-knockout (KO) cells, as shown by Western blotting (b). The level of IFN-α-mediated enhancement as measured in the oxLDL-treated TDMs was significantly lower in the CMPK2-KO cells, compared to the wild-type controls (c). Analysis with BODIPY revealed results consistent with the results from oil red O staining (d). The uptake of Dil-oxLDL induced by IFN-α treatment was reduced in the CMPK2-KO cells (e). IFN-α-induced expression of SR-A was determined by Western blotting (f). IFN-α-induced expression of CMPK2 in mitochondrial and cytosolic fractions of cellular lysates was determined by Western blotting (g, the results from 3 independent experiments were shown in Supplementary Figure 5). Asterisks indicate values that are significantly different from the relevant control (*P < 0.05)

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