Fig. 4

NF-κB mediates inflammation-induced PTPR-γ expression. a Ptprg mRNA level in HepG2 cells and b C2C12 cells treated as indicated. (IκBα DN expresses a mutant “super-repressor” allele of IκBα harboring two amino acid substitutions: Serine 32 and 36 are substituted in Alanine). c ChIP analyses of NF-κB in C2C12 cells treated with LPS or vehicle (relative data are represented over IgG controls). d, e ChIP analyses of NF-κB in liver of mice treated with saline or LPS and STD or HCD (relative data are represented over IgG controls). f, g mRNA levels of Firefly luciferase in HepG2 and C2C12 cells transduced with pGL2-basic plasmid containing Ptprg promoter region containing a mutated/disrupted NF-κB putative binding motif and treated as indicated. h Knockdown in HepG2 cells of SIRT1 using two different siRNAs and i Ptprg mRNA level in the same cells. j, k Ptprg mRNA level in HepG2 and C2C12 cells treated with resveratrol as indicated. l Insulin tolerance test (ITT) in 12-week-old mice treated 28 days with LPS (the dose of insulin injected intra-peritoneally is 0.75 U/kg). Error bars represent SEM. Statistical analyses were done using two-tailed unpaired Student’s t test or using one-way ANOVA (Tukey’s post test). ^* P < 0.05, ^** P < 0.01, ^*** P < 0.001. See also Supplementary Fig. 6