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Fig. 7 | Journal of Nanobiotechnology

Fig. 7

From: UTX deletion promotes M2 macrophage polarization by epigenetically regulating endothelial cell-macrophage crosstalk after spinal cord injury

Fig. 7

UTX directly regulate miR-467b-3p and inhibit the expression of PTEN. A A schematic illustration of the UTX, H3K27me3/me2 and miR-467b-3p/Smfbt2 promoter forming an epigenetic regulation complex. B The overexpression efficiency of UTX verified by qRT-PCR. C The expression levels of miR-467b-3p in UTXf/f ECs, UTX−/− ECs and UTXf/f-ECs + UTX OE. D The mRNA expression levels of UTX after miR-467b-3p mimic and inhibitor conducted to ECs. E Chip-qPCR detection of the rate of H3K27 binding to miR-467b-3p/Sfmbt2 promotor. F Overlap analysis of predicted potential target proteins of miR-467b-3p from the TargetScan database and miRWalk database. G KEGG signaling pathway enrichment analysis. H qRT-PCR analysis of the mRNA expression levels of candidate target proteins after miR-467b-3p mimic transfected macrophages. I Western blotting analysis of the levels of PTEN, AKT and AKT2 after miR-467b-3p mimic transfected macrophages. J–M Statistical analysis of PTEN, AKT and AKT2 expression levels in I. N Schematic diagram of the binding site of miR-467b-3p to PTEN mRNA. O, P Dual luciferase reporter assay to detect luciferase activity in wild-type (Wild) and mutant (Mutant) PTEN loci after miR-467b-3p mimic transfection of HEK-293T cells. nsP > 0.05, **P < 0.01 vs. corresponding control groups. n = 6/per group

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