Skip to main content
. 2021 Aug 17;62(9):858–867. doi: 10.3349/ymj.2021.62.9.858

Fig. 5. NEAT1 directly regulated miR-9-5p/ SLC26A2. (A) Schematic representation of the miR-9-5p putative binding site in the NEAT1 3′-UTR. (B) Luciferase reporter assays showed that miR-9-5p overexpression remarkably reduced the luciferase activity of NEAT1-wt-containing vector, whereas it had no effect on the NEAT1-mut-containing vector. (C) The expressions of NEAT1 and miR-9-5p bound to Ago2 or IgG were detected by RIP and qRT-PCR. (D) qRT-PCR showed miR-9-5p level in PDGF-induced HASMCs transfected with siNEAT1or oe-NEAT1. (E) Western blotting showed SLC26A2 expression in PDGF-induced HASMCs treated with miR-9-5p mimic or miR-9-5p mimic+oe-NEAT1. Data are presented as the mean±SD of three independent experiments. *p<0.05, compared to their respective NCs, p<0.05, compared to IgG group. HASMCs, human airway smooth muscle cells; PGDF, platelet-derived growth factor; NC, negative control.

Fig. 5