Fig. 3

PVT1 acts as s sponge for miR-128-3p to facilitate Sp1 expression. a Compared with the SR group, the AF group showed significantly decreased expression of miR-128-3p (a) and increased mRNA (b) and protein (c) expression of Sp1 in human atrial muscle tissues. β-actin served as the loading control. d PVT1 expression was negatively correlated with miR-128-3p expression, whereas positively correlated with Sp1 mRNA expression in human atrial muscle tissues from AF patients. e The predicted binding sites between PVT1 and miR-128-3p (DIANA TOOLS-LncBase v.2). f Relative PVT1 and miR-128-3p expression presented as fold enrichment in Ago2 relative to normal IgG immunoprecipitates. RIP assays disclosed that PVT1 and miR-128-3p expressions were substantially enriched by Ago2 antibody compared with control IgG antibody. g Luciferase activity was measured in fibroblasts co-transfected with mimic NC or miR-128-3p mimic and PVT1-wt or PVT1-mut reporter at 48 h after transfection. PVT1 interacted directly with miR-128-3p. In addition, PVT1 overexpression inhibited miR-128-3p expression (h), elevated mRNA (i) and protein (j) levels of Sp1 in fibroblasts, whereas PVT1 knockdown exerted the opposite effect. a-c ^*P < 0.05 vs. SR; (f) ^*P < 0.05 vs. anti-IgG; (g) ^*P < 0.05 vs. PVT1 wt + mimic NC, ^#P < 0.05 vs. PVT1 wt + control; h-j ^*P < 0.05 vs. vector, ^#P < 0.05 vs. si-Ctrl. Data are presented as mean ± SD. SR, sinus rhythm; AF, atrial fibrillation; PVT1, plasmacytoma variant translocation 1; Sp1, specificity protein 1