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. 2022 Jul 22;7(14):e158428. doi: 10.1172/jci.insight.158428

Figure 7. Depletion of CTNND1 in HRECs inhibits in vitro EC angiogenesis and cell proliferation partially through inactivation of Wnt signaling activity.

Figure 7

(A) Quantification of relative CTNND1, CCND1, MYC, JUN, DKK1, CD44, and CLDN5 mRNA levels detected by RT-qPCR in Ctrl and CTNND1-KD HRECs. Error bars, SDs. Student’s t test (n = 3), ****P < 0.0001. (B) Western blot analysis of protein levels of Wnt signaling targets (p120, CyclinD1, c-Myc, and GLUT1) in Ctrl and CTNND1-KD HRECs. (C–E) Quantification of relative CyclinD1, c-Myc, and GLUT1 protein levels in Ctrl and CTNND1-KD HRECs. Error bars, SDs. Student’s t test (n = 3), *P < 0.05, ***P < 0.001, ****P < 0.0001. (F) Representative bright-field images of in vitro tube formation in Ctrl and CTNND1-KD HRECs. Scale bars, 25 μm. (G) Representative immunofluorescence images of Ctrl and CTNND1-KD HRECs labeled with EdU (red) and DAPI (blue). Scale bars, 50 μm. (H) Quantification of the percentage of EdU+ nuclei in Ctrl and CTNND1-KD HRECs. Error bars, SDs. Student’s t test (n = 5), ***P < 0.001. Experiments were performed at least 3 times independently.