Fig. 6

Perisotin/NAP1L2 blunted BCAA catabolism in CF. A Enrichment analysis chord diagram showing the BCAA catabolism was impaired in hearts after periostin OE. B Branched-chain amino acid catabolism (R-MMU-70895).gsea. C Branched-chain amino acid catabolism (R-MMU-70895) Heatmap of the Analyzed GeneSet. D Serum and cardiac BCAA levels in mice without periostin. E Serum and cardiac BCAA levels in mice with periostin OE. F Representative mRNA levels of BCAT2, BCKDHA, BCKDK, and PP2Cm in hearts from mice without periostin. G Representative mRNA levels of BCAT2, BCKDHA, BCKDK, and PP2Cm in hearts from mice with periostin OE. H Representative blots and quantitation of BCAT2 and PP2Cm in CF after silencing NAP1L2. I Representative blots and quantitation of BCAT2 and PP2Cm in CF after treatment with ADTL-SA1215 (5 μM), an agonist of SIRT3. J Representative blots and quantitation of H3K27me2, H3K36me2, H3K79me3, H3K27ac, H3K14ac, and H3K9ac in CF upon NAP1L2 overexpression. K H3K27acoccupancy at the promoters of BCAT2 and PP2Cm in CF transfected with NAP1L2 OE plasmid by ChIP. n = 3–4. *P < 0.05 versus Con, Con siRNA or Vector, †P < 0.05 versus HG or Diabetes. The P-value was calculated by unpaired two-tailed Student’s t-test (K). Differences between groups were assessed with ANOVA followed by Bonferroni post-hoc test (D–I)