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Fig. 6 | Molecular Medicine

Fig. 6

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

Fig. 6

USP14 depletion repressed EndMT via inactivation of NLRC5/Smad2/3 pathway. The HUVECs were transfected with sh-USP14 combined with or without oe-NLRC5, followed by exposure to 100 µg/mL ox-LDL for 24 h. (A) RT-qPCR analysis of USP14 expression levels. (B) The abundance of USP14, NLRC5, Smad2, p-Smad2, Smad3, p-Smad3 was assessed by Western blotting. Expression of EndMT markers CD31, VE-Cadherin, α-SMA, and vimentin were measured by Western blotting (C) and immunofluorescence staining (D) (scale bar = 25 μm). (E) Concentrations of IL-6 and TNF-α produced by HUVECs were evaluated by ELISA kits. (F)&(G) Migration of HUVECs was evaluated by transwell and scratch assays. n = 3. *p < 0.05, **p < 0.01, ***p < 0.001

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