Fig. 8 | Nature Communications

Fig. 8

From: miR-103 promotes endothelial maladaptation by targeting lncWDR59

Fig. 8

Human lncWDR59 conserved role in vitro and in human plaques. a Gene locus and full transcript of human lncWDR59 (hsa-lncWDR59) sequence on chromosome 16 between FA2H and WDR59 genes. b Enrichment of hsa-lncWDR59 transcripts in the RISC complex after transfection of human aortic ECs (HAoECs) with miR-103 or control mimics together with a mutant form of Ago2, following an immunoprecipitation of GW182 protein (GW182-IP). Results of three experiments are shown. GAPDH was used as housekeeping gene and for relative expression analysis. c Analysis of Ki67 immunostaining and MN formation in HAoECs transfected for 48 h with hsa-lncWDR59 gapmers (hGlncWDR59). Data are normalized and expressed as percentage of the total number of cells (n = 4 per group). d In situ hybridization for miR-103 and lncWDR59 on human plaques. Areas lacking of lesions were used as control areas. vWF and DAPI were used to stain ECs and nuclei, respectively (n = 4 per group). e Correlation of the relative expression levels of hsa-lncWDR59 in human carotid lesions with necrotic core area, SOX17 expression, and Ki67 endothelial staining (Ki67+vWF+), (n = 17–20 per group). *P < 0.05 by Student’s t-test and a compute nonparametric Spearman's rho correlation analysis. Scale bar: 25 µm

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