Fig. 4

PVT1 promotes atrial fibrosis by regulating the TGF-β1/Smad signaling pathway via the miR-128-3p/Sp1 axis. a The predicted binding site between miR-128-3p and 3′-UTR of Sp1 (Targetscan). b Luciferase assay confirmed that Sp1 was a target of miR-128-3p. miR-128-3p mimic significantly suppressed PVT1 expression (c), and the mRNA and protein expression of Sp1 (d). miR-128-3p inhibitor exerted the opposite effect. e miR-128-3p mimic significantly reversed the PVT1 overexpression-induced Sp1 expression, at both mRNA and protein levels. Effect of miR-128-3p mimic and Sp1 silencing on the PVT1 overexpression-induced fibroblasts proliferation (f), collagen production, and TGF-β1/Smad signaling activation (g) was shown. b ^*P < 0.05 vs. Sp1 wt + mimic NC; (C-D) ^*P < 0.05 vs. mimic NC, ^#P < 0.05 vs. inhibitor NC; (e) ^*P < 0.05 vs. vector, ^#P < 0.05 vs. PVT1 + mimic NC; (f-g) ^*P < 0.05 vs. Ang-II + vector, ^#P < 0.05 vs. Ang-II + PVT1 + mimic NC, ^$P < 0.05 vs. Ang-II + PVT1 + si-Ctrl. Data are presented as mean ± SD. Sp1, specificity protein 1; PVT1, plasmacytoma variant translocation 1; TGF-β1, transforming growth factor-β1