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. 2021 Sep 7;22(5):1271. doi: 10.3892/etm.2021.10706

Figure 4.

Figure 4

Silencing TFEC abolishes AngII-induced cardiomyocyte hypertrophy. (A) Compared with the control, treatment with AngII increased the relative cardiomyocyte size (magnification, x40). (B) mRNA levels of ANP, BNP and β-MHC were significantly increased in primary cardiomyocytes treated with AngII compared with the control. (C) In primary cardiomyocytes, treatment with AngII significantly increased the expression of TFEC compared with treatment with the control. (D) Transfection with rAd-sh-TFEC significantly decreased the expression of TFEC even in primary cardiomyocytes treated with AngII. (E) AngII-induced increase in cardiomyocyte size could be reversed by TFEC knockdown in primary cardiomyocytes (magnification, x40). (F) Elevated mRNA levels of ANP, BNP and β-MHC induced by AngII could be partially abolished following TFEC knockdown in primary cardiomyocytes. *P<0.05, **P<0.01 and ***P<0.001. AngII, angiotensin II; Con, control; NC, negative control; ANP, atrial natriuretic peptide; BNP, brain natriuretic peptide; β-MHC, β-myosin heavy chain; TFEC, transcription factor EC; sh, short hairpin.