Research Paper Volume 13, Issue 3 pp 3588—3604

Downregulation of circFASTKD1 ameliorates myocardial infarction by promoting angiogenesis

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Figure 2. CircFASTKD1 binds directly to miR-106a. (A) Schematic diagrams of the circFASTKD1-WT and -Mut luciferase reporter vectors. (B) A dual-luciferase reporter assay was performed in 293T cells to verify that miR-106a was a sponged target of circFASTKD1. (C) CircFASTKD1 levels in the nuclear and cytoplasmic fractions of HUVECs were analyzed using qRT-PCR. (D) The colocalization of miR-106a with circFASTKD1 in HUVECs was detected with a FISH assay. (E) The association between circFASTKD1 and Ago2 was detected with a RIP assay using an Ago2 or IgG antibody. CircFASTKD1 levels in HUVECs were assessed using qRT-PCR. (F) The associations among circFASTKD1, miR-106a and Ago2 were detected with a RIP assay using an Ago2 or IgG antibody. MiR-106a levels in HUVECs were assessed using qRT-PCR. (G) MiR-106a levels were detected via qRT-PCR in HUVECs transfected with circFASTKD1 or control (Ctrl) vectors. (H) MiR-106a levels were detected via qRT-PCR in HCMECs transfected with sh-circFASTKD1 or sh-NC. Data are presented as the mean of three experiments, and the error bars represent the SD (*P<0.05 and **P<0.01).