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. 2022 Mar 1;43:187–203. doi: 10.1016/j.jare.2022.02.017

Fig. 5.

Fig. 5

SOX4 overexpression in endothelial cells. (A) Western blotting on isolated ECs from ApoE−/− mice, previously subjected to tail vein injection of endothelial-specific AAV-SOX4 (n = 6 per group). (B, C) Oil red O staining on atherosclerotic lesions of (B) en face aortae and (C) aortic roots of AAV-SOX4-injected ApoE−/− mice (n = 6 per group; Scale bar: 500 μm). (D) Immunofluorescence staining on endothelial and mesenchymal markers of mouse aortic roots (n = 6 per group; Scale bar: 500 μm). (E, F) Western blotting on Ad-SOX4-treated (E) HUVECs and (F) HAECs (n = 6 per group). (G) Immunofluorescence staining on endothelial and mesenchymal markers of Ad-SOX4-infected HUVECs (n = 6 per group; Scale bar: 50 μm). (H) Morphology of Ad-SOX4-treated HUVECs (L/W ratio: Feret value/Min Feret value; Scale bar: 100 μm). (I) Functional assay on endothelium-dependent relaxation of Ad-SOX4-infected C57BL/6 mouse aortae by wire myograph (n = 6 per group). Data are presented as mean ± SD. *P < 0.05 vs AAV-Vector or Ad-Vector (unpaired t-test and nonparametric Mann-Whitney test). ACh, acetylcholine; HAEC, human aortic endothelial cell; HUVEC, human umbilical vein endothelial cell; Phe, phenylephrine. (For interpretation of the references to colour in this figure legend, the reader is referred to the web version of this article.)