Fig. 7

RIMKLA inhibits FASn and CD36 expression by blocking Hcy-induced AP1 activation. a AP1 overexpression upregulated FASn and CD36 protein levels in mouse hepatocytes. Cells were transfected with plasmid for 24 h before assays. n = 5–6. b Hcy activated AP1 in mouse hepatocytes. Cells were treated with various Hcy concentrations (100 µM, 500 µM) for 24 h before assays. n = 6. c Hcy-induced FASn and CD36 expressions were blocked by AP1 inhibitor in mouse hepatocytes. Cells were treated with 100 μM Hcy in the absence or presence of 20 μM AP1 inhibitor (SR11302) for 24 h before assays. n = 6. d–e AP1 was activated in the livers of obese mice. n = 7. f RIMKLA overexpression repressed AP1 phosphorylation in mouse livers fed on HFD for 3 months. n = 6. g RIMKLA overexpression repressed AP1 phosphorylation in cultured mouse hepatocytes. n = 7. h siRNA silencing of BHMT1 increased the transcriptional activities of both FASn and CD36 promoters. n = 6. i Silencing of BHMT1 blunted RIMKLA-induced inhibition on Hcy content in mouse hepatocytes. n = 5–6. j Silencing of BHMT1 inhibited RIMKLA’s repression on AP1 phosphorylation, and FASn and CD36 expressions in mouse hepatocytes. n = 5. k Silencing of BHMT1 abolished RIMKLA-inhibition on lipid deposition in mouse hepatocytes in the presence of fatty acids (0.1 mM oleic acid+0.2 mM palmitic acid). n = 5. Scale bar: 50 µm. All data were represented as mean ± SEM. Statistical P values were marked in each panel. P values for (a, d–g, h) were calculated by student’s t-test, for (b, c, i–k) were analyzed using one-way ANOVA followed by Bonferroni’s post hoc analysis