Research Paper Volume 13, Issue 9 pp 12919—12928

Knockdown of ZFAS1 improved the cardiac function of myocardial infarction rats via regulating Wnt/β-catenin signaling pathway

Knockdown of ZFAS1 significantly promoted the cell viability. (A) The expression of ZFAS1 was measured in the MI model. (B) The expression of ZFAS1 was measured in the hypoxia cell model. (C) Knockdown of ZFAS1 markedly promoted the ability of cell proliferation. (D) Cell migration was measured using wound healing method (Scale bar = 500 μm). (E) Knockdown of ZFAS1 markedly promoted cell migration compared with group hypoxia. (F) Cell invasion was measured using Transwell method (Scale bar = 200 μm). (G) Knockdown of ZFAS1 markedly promoted t cell invasion compared with group hypoxia. *P #P

Figure 1. Knockdown of ZFAS1 significantly promoted the cell viability. (A) The expression of ZFAS1 was measured in the MI model. (B) The expression of ZFAS1 was measured in the hypoxia cell model. (C) Knockdown of ZFAS1 markedly promoted the ability of cell proliferation. (D) Cell migration was measured using wound healing method (Scale bar = 500 μm). (E) Knockdown of ZFAS1 markedly promoted cell migration compared with group hypoxia. (F) Cell invasion was measured using Transwell method (Scale bar = 200 μm). (G) Knockdown of ZFAS1 markedly promoted t cell invasion compared with group hypoxia. *P < 0.05 compared with the group control or sham. #P < 0.05 compared with the group hypoxia.