Fig. 2 | Nature Communications

Fig. 2

From: miR-103 promotes endothelial maladaptation by targeting lncWDR59

Fig. 2

Screening of miR-103 target lncRNAs expression and identification of lncWDR59 as target of miR-103. qPCR for miR-103 target lncRNAs expression in different cells or conditions, such as a MAoECs and BMDM (n = 3–5 per group), b MAoECs under high or low shear stress (HSS or LSS) conditions for 48 h (n = 3 per group), c MAoECs treated with oxidized LDL (oxLDL) for 24 h (n = 4 per group), d aortic arches (Arch) and thoraco-abdominal (Thoracoabd) aortas from 12-week normal diet-fed Apoe−/− mice (n = 5–10 per group), e all aorta from Apoe−/− mice fed 12 weeks of normal diet (ND) or high-fat diet (HFD) (n = 3–5 per group), and f ECs and plaques isolated from Apoe−/− mice fed 4 weeks an HFD using the laser microdissection system (n = 3–7 per group). g In situ hybridization for miR-103 and lncWDR59 on 12 weeks HFD-fed EC-DicerWT and EC-Dicerflox mice. vWF and DAPI were used to stain ECs and nuclei, respectively (n = 4 mice per group). h The 6-mer seed predicted binding site for miR-103 on lncWDR59 transcript predicted using RNAHybrid and the sequence of the competitive TSB, which specifically inhibits the binding of miR-103 on lncWDR59 transcript (n = 3–8 per group). Non-classical Watson and Crick interactions between A and U were represented with a dot. B2m was used as housekeeping gene for relative quantification. EC endothelial cells, MAoECs murine aortic ECs, BMDM bone marrow-derived macrophages, TSB target site blocker. Data are represented as mean ± SEM of the indicated number (n) of repeats. *P < 0.05, **P < 0.01, and ***P < 0.001 by Student’s t-test. Scale bar: 25 µm

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