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Fig. 4 | Journal of Translational Medicine

Fig. 4

From: Upregulation of miR-483-3p contributes to endothelial progenitor cells dysfunction in deep vein thrombosis patients via SRF

Fig. 4

SRF is a validated target of miR-483-3p. a SRF is a putative target of miR-483-3p. Putative binding sites of miR-483-3p in the SRF 3′UTR predicted by TargetScan among different mammalian species. b Putative binding sites of hsa-miR-483-3p in the human SRF 3′UTR (white sequences) predicted by TargetScan. c Schematic graph of the constructed reporter plasmid containing putative binding sites of hsa-miR-483-3p in the SRF 3′UTR. SRF-3′UTR mut indicates the SRF-3′UTR with mutation in miR-483-3P-binding site. The mutated nucleotides in SRF-3′UTR fragments are underlined. d Dual luciferase report assays were performed on HEK 293 T cells. Each bar represents mean values ± SEM (n = 3, **P < 0.01). e The protein level of SRF in EPC transfected with miR-483-3p agomir and antagomir. Each bar represents mean values ± SEM (n = 3, *P < 0.05 vs. negative control; **P < 0.01 vs. negative control). f The protein level of SRF in EPC transfected with miR-483-3p agomir and SRF, SRF siRNA. Each bar represents mean values ± SEM (n = 3, **P < 0.01 vs. negative control). g miR-483-3p expression was measured in healthy control and patients with DVT by quantitative real-time PCR. Data are expressed as mean ± SEM (n = 10, ***P < 0.01 vs. health control). h The protein level of SRF in patients with DVT and health control. Each bar represents mean values ± SEM (n = 10, *P < 0.05 vs. health control)

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