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. 2020 Oct 31;29(3):1120–1137. doi: 10.1016/j.ymthe.2020.10.024

Figure 5.

Figure 5

miR-30b-3p Was the Downstream of lncRNA Gm15834 and Regulated Cardiac Hypertrophy via Regulating Autophagy

(A) Fluorescence in situ hybridization (FISH) was performed to detect the subcellular localization of lncRNA Gm15834. Scale bar, 20 μm. (B) Venn diagram of miR-30b-3p in 3 miRNA expression datasets of cardiac hypertrophy or heart failure. (C) qRT-PCR results of miR-30b-3p expression in TAC models and Ang-II induced models in vitro. ∗p < 0.05 versus sham/control group. n = 3. (D) qRT-PCR results of miR-30b-3p expression in lncRNA Gm15834 interference experiments. ∗p < 0.05 versus NC/pcDNA group. n = 3. (E) The binding sites between miR-30b-3p and lncRNA Gm15834, including the binding site of the conserved region. (F and G) Western blot results of β-MHC (F) and BNP (G) protein expression in miR-30b-3p overexpression and antagonism groups. ∗p < 0.05 versus control group; #p < 0.05 versus Ang-II group; @p < 0.05 versus Ang-II + miR-30b group. n = 6. (H) Immunofluorescence results of cardiomyocyte areas from in vitro groups. ∗p < 0.05 versus control group; #p < 0.05 versus Ang-II group; @p < 0.05 versus Ang-II + miR-30b group. n = 3. Scale bar, 50 μm. (I) In vitro transfection of double-labeled LC3 autophagy adenovirus to count autolysosomes and autophagosomes from cardiomyocytes. ∗p < 0.05 versus control group; #p < 0.05 versus Ang-II group; @p < 0.05 versus Ang-II + miR-30b group. n = 3. Scale bar, 20 μm. (J–L) Western blot results of LC3-II (J), Beclin-1 (K), and p62 (L) protein in miR-30b-3p overexpression and antagonism groups. ∗p < 0.05 versus control group; #p < 0.05 versus Ang-II group; @p < 0.05 versus Ang-II + miR-30b group. n = 6.