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. 2020 Feb 19;11:78. doi: 10.3389/fgene.2020.00078

Figure 4.

Figure 4

Overexpression of miR-26b-5p, miR-204-5p, and miR-497-3p attenuates IGF-1 induced cardiomyocyte hypertrophy. (A, B), The morphology of H9C2 cells treated with IGF-1 (10 µM)for 48 h. (C), The messenger RNA (mRNA) levels of atrial natriuretic polypeptide (ANP), brain natriuretic peptide (BNP), and α-actin in H9C2 cells treated with IGF-1 (10 µM). (D, E), The protein expression of autophagy maker (LC3B, Beclin1, and SQSTM1) of H9C2 cells treated with IGF-1 (10 µM). (F, G), Cardiomyocyte surface area of H9C2 cells in response to IGF-1 (10 µM) with adenovirus-mediated microRNA (miRNA) infection. (H–J) mRNA levels of cardiomyocyte hypertrophy makers of H9C2 cells treated with IGF-1 (10 µM) and adenovirus mediated miRNAs. (K–N) Protein levels of cardiomyocyte hypertrophy makers of H9C2 cells treated with IGF-1 (10 µM) and adenovirus mediated miRNAs. ** P < 0.01, IGF+scramble (n=6) vs. CON+scramble group (n=6). #P < 0.05, ## P < 0.01, miRNA adenovirus intervention group (n=6) vs. IGF-1+scramble group (n=6). Data are presented as means ± SD. Statistical significance was evaluated with the two-tailed Student's t test (B, C, E) and one-way analysis of variance with Bonferroni post-hoc analysis (G–J, L–N).