Figure 8: MiR-19a-3p/19b-3p decreases expression of autophagy-related fibrosis members induced by TGF-β1. | Scientific Reports

Figure 8: MiR-19a-3p/19b-3p decreases expression of autophagy-related fibrosis members induced by TGF-β1.

From: Autophagy inhibition of hsa-miR-19a-3p/19b-3p by targeting TGF-β R II during TGF-β1-induced fibrogenesis in human cardiac fibroblasts

Figure 8

(a) Human cardiac fibroblasts were pre-transfected with miR-19a-3p/19b-3p and miR Control. Then cells were treated with TGF-β1 (10 ng/ml) for the indicated duration. LC3-I, LC3-II, p62/SQSTM1, collagen I α2, fibronectin, MMP-9, and MMP-2 levels were measured in whole-cell lysates. Protein loading was confirmed using GAPDH. (b,c) Quantitative data of densitometric analyses. The ratios of LC3-I, LC3-II, p62/SQSTM1, collagen I α2, fibronectin, MMP-9, and MMP-2 to GAPDH were present as mean ± SEM, n = 3, *p < 0.05, **p < 0.01 vs. group of miR Control and TGF-β1 co-treatment. (d) Rapamycin reverses the inhibition effect of miR-19a-3p/19b-3p on TGF-β1-induced autophagy-related fibrosis. Human cardiac fibroblasts were transfected with miR-19a-3p/19b-3p and miR Control. Then cells were pretreated with rapamycin (4 hours, 1 μM) and co-treated with TGF-β1 (10 ng/ml) for the indicated duration. LC3-I, LC3-II, p62/SQSTM1, collagen Iα2, fibronectin, MMP-9, and MMP-2 levels were measured in whole-cell lysates. Protein loading was confirmed using GAPDH. (e,f) Densitometry analysis showed that rapamycin (1 μM) significantly reversed the inhibition of miR-19a-3p/19b-3p on TGF-β1-induced autophagy-related fibrosis in human cardiac fibroblasts. *p < 0.05, **p < 0.01 vs group of miR Control and TGF-β1 co-treatment; ##p < 0.01 vs group of miR 19a-3p and TGF-β1 co-treatment; $$p < 0.001 vs group of miR 19b-3p and TGF-β1 co-treatment.

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