Figure 6.

KSRP mediates the protective effects on inflammation activation, insulin resistance and atherosclerosis in FBXW2 deficiency mice. FBXW2^fl/flLysm^Cre‐/− or FBXW2^fl/flLysm^Cre+/− mice received an injection of lentivirus encoding shRNA against KSRP and then were fed with HFD for 12 weeks (n = 15). Fasted mice were then subjected to the A) GTT and B) ITT. C) Acute insulin signaling in epididymal fat (epiWAT), the soleus, and the liver were detected by immunoblot analysis of AKT phosphorylation. D) Representative images of CD68 immunohistochemistry in epiWAT sections. Scale bars, 50 µm. The relative quantification of the adipocyte area and CD68 level are shown. Relative mRNA levels of inflammatory factors (IL‐1β, iNOS, TNFα, CCL2 and IL‐6) in E) epiWAT and F) the liver of mice. G) The plasma concentrations of factors (IL‐1β, CCL2, TNFα and IL‐6) in the mice were tested. ApoE^−/−FBXW2^fl/flLysm^Cre‐/− and ApoE^−/−FBXW2^fl/flLysm^Cre+/− mice received an injection of lentivirus encoding shRNA against KSRP and then were fed a WD for 10 weeks (n = 15). H) Representative CD68⁺ immunofluorescence staining and quantitation in the plaques of aortic root. Scale bars, 200 µm. I) Relative mRNA levels of inflammatory mediators (TNFα, IL‐1β, iNOS, CCL2 and IL‐6) in the aortas of mice. The data are analyzed by ANOVA with the post‐hoc test and are presented as the mean ± SEM. *p < 0.05 and ^# p < 0.05.