Fig. 2

EndMT was induced in the in vivo and in vitro models of atherosclerosis. ApoE^–/– mice fed with high-fat diet was used as the mouse model of atherosclerosis. Normal chow-fed diet (NFD) represents normal mice. High-fat diet (HFD) represents atherosclerosis mice. (A) Expressions of CD31, α-SMA, USF1 and USP14 in aortas of ApoE^–/– mice were determined by RT-qPCR. (B) Immunofluorescence staining of CD31 and α-SMA in the aortas of ApoE^–/– mice (scale bar = 50 μm). (C) Atheromatous plaque formation, collagen accumulation, and lipid deposition were observed by HE, Masson, and Oil red O staining (scale bar = 50 μm). (D) IL-6, TNF-α and IL-1β levels in serum of mice were determined using ELISA kits. (E) Western blotting analysis of CD31, VE-Cadherin, α-SMA and vimentin levels in the aortas. ox-LDL-exposed HUVECs were used as the in vitro model of atherosclerosis. (F) The morphological changes of HUVECs were observed (scale bar = 100 μm). (G) CD31 and α-SMA expression in HUVECs was determined by immunofluorescence staining (scale bar = 25 μm). (H) Protein abundance of CD31, VE-Cadherin, α-SMA and vimentin in HUVECs was measured by Western blotting. (I) Concentrations of IL-6 and TNF-α in supernatant of HUVECs was detected using ELISA kits. For A-E, n = 6; for G-I, n = 3. *p < 0.05, **p < 0.01, ***p < 0.001