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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. 5. — Identification of STAT3 as a novel target for miR-328-3p. (a) Schematic representation of the putative miR-328-3p binding site in the STAT3 3′-UTR. (b) Luciferase assays were conducted to assess miR-328-3p targeting of the STAT3 3′-UTR. (c) The STAT3 expression level was downregulated by miR-328-3p overexpression but upregulated by miR-328-3p inhibitor in PDGF-induced hPAECs. (d and e) Detection of effects of circHIPK3 knockdown on mRNA and protein expression of STAT3 in PDGF-induced hPAECs via qPCR and western blot. 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; STAT3: STAT3 overexpression vector pcDNA-STAT3; NC: negative control.