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Fig. 7 | Molecular Medicine

Fig. 7

From: USF1 transcriptionally activates USP14 to drive atherosclerosis by promoting EndMT through NLRC5/Smad2/3 axis

Fig. 7

Inactivating Smad2/3 pathway ameliorated atherosclerosis via inhibiting EndMT in vivo. ApoE–/– mice were fed with the Western high-fat diet for 3 months. SB431542 (4.2 mg/kg) was daily intraperitoneally injected into mice during experimental period. Normal chow-fed diet (NFD) represents normal mice. High-fat diet (HFD) represents atherosclerosis mice. (A) Western blotting analysis of USF1, USP14, NLRC5, Smad2, p-Smad2, Smad3, p-Smad3 levels in the aortic tissues. (B) The atheromatous plaque formation and collagen accumulation in the aortas was determined by HE and Masson staining (scale bar = 50 μm). (C) The aortic lipid deposition was assessed by Oil red O staining. (D) The morphological changes was evaluated by EVG staining. (E) Immunofluorescence staining of CD31 and α-SMA in the aortas of ApoE–/– mice (scale bar = 50 μm). (F) The release of IL-6, TNF-α and IL-1β in serum was measured by ELISA kits. (G) Western blotting analysis of CD31, VE-Cadherin, α-SMA and vimentin levels in aortas. n = 6. **p < 0.01, ***p < 0.001

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