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. 2021 Mar 29;11(2):20458940211000234. doi: 10.1177/20458940211000234

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© The Author(s) 2021

Creative Commons Non Commercial CC BY-NC: This article is distributed under the terms of the Creative Commons Attribution-NonCommercial 4.0 License (https://creativecommons.org/licenses/by-nc/4.0/) which permits non-commercial use, reproduction and distribution of the work without further permission provided the original work is attributed as specified on the SAGE and Open Access pages (https://us.sagepub.com/en-us/nam/open-access-at-sage).

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Fig. 4. — CircHIPK3 binding with miR-328-3p. (a) The expression level of miRNAs in PDGF-treated hPAECs was detected by qRT-PCR. (b) The expression level of miR-328-3p in hPAECs was downregulated after PDGF treatment. CircHIPK3 knockdown reversed this effect. (c) The putative binding sites between circHIPK3 and miR-328-3p and the mutant sites in circHIPK3-MUT reporter were displayed. (d) Luciferase activity was detected in 293T cells cotransfected with circHIPK3-WT or circHIPK3-MUT reporter and miR-328-3p mimics or miR-328-3p inhibitor. (e) RNA immunoprecipitation assays demonstrated that circHIPK3 was directly binding to miR-328-3p. Data were expressed as mean ± SD in three independent experiments. **P < 0.01, ***P < 0.001. PGDF: platelet-derived growth factor; hPAEC: human pulmonary artery endothelial cell; GADPH: glycerldehyde-3-phosphate dehydrogenase; NC: negative control; IgG: immunoglobulin.