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. 2021 Feb 6;39(5):581–599. doi: 10.1002/stem.3332

FIGURE 2.

FIGURE 2

Upregulation of Smurf2 promoted angiogenesis by mesenchymal stem cells (MSCs) in patients with ankylosing spondylitis (ASMSCs). A‐C, Compared to those in the MSCs in patients with healthy donors (HDMSCs), the levels of both Smurf2 mRNA and protein were increased in ASMSCs. Lentiviruses were used to silence or overexpress Smurf2 or C716A (catalytically inactive mutant of Smurf2) in both HDMSCs and ASMSCs. D,E, The interference efficiency of shRNA targeting Smurf2 and the overexpression efficiency of OE‐Smurf2 and OE‐C716A were both verified by Western blot analyses. F‐I, In the CCK‐8 (fifth day), wound healing and Transwell assays, Smurf2 knockdown decreased human umbilical vein endothelial cell (HUVEC) proliferation and migration, whereas Smurf2 overexpression exerted the opposite effect, but C716A overexpression did not induce a similar phenotype. Scale bar = 250 μm. J‐M, Smurf2 knockdown in MSCs decreased HUVEC tube formation, whereas overexpression of Smurf2 in MSCs increased HUVEC tube formation, with no notable difference between HDMSCs and ASMSCs. However, overexpression of C716A did not exert a significant effect on the HDMSCs or ASMSCs. The cell‐covered area, total tube length, total branch points and total loops were quantified. n = 10 different HDMSC or ASMSC lines per group. All data are presented as the means ± SD. *P < .05, **P < .01, ***P < .001. n.s., not significant