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. 2016 May 3;311(1):H64–H75. doi: 10.1152/ajpheart.00151.2016

Fig. 9.

Fig. 9.

Role of miR-33a in TXNIP deficiency-mediated induction of β-oxidation enzymes. A: confirmation of effective and persistent TXNIP knockdown in H9C2 cardiomyocytes with and without miR-33a overexpression. Protein expression levels of the fatty acid oxidation enzymes CROT (B), CPT1a (C), and HADHB (D), as well as of AMPKα and p-AMPKα (E) and p-ACC2 (F), as assessed by immunoblotting and corrected for actin in H9C2 cardiomyocytes with TXNIP knockdown (siTXNIP) or TXNIP knockdown and miR-33a overexpression (siTXNIP+miR-33a) and compared with cells transfected with scrambled control (scramble). Representative immunoblots and means ± SE of three independent experiments are shown. **P < 0.005; ***P < 0.001; N.S., not significant (one-way ANOVA).