Research Paper Volume 13, Issue 3 pp 3588—3604

Downregulation of circFASTKD1 ameliorates myocardial infarction by promoting angiogenesis

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Figure 1. Function of circFASTKD1 in angiogenesis in vitro. (A) CircFASTKD1 levels were determined via qRT-PCR in HUVECs, HBMECs, HMVECs, HMEC-1 cells and HCMECs. (B) Structures of the control (Ctrl), circFASTKD1 and sh-circFASTKD1 vectors. (C, D) CircFASTKD1 levels were determined via qRT-PCR in HUVECs transfected with the Ctrl or circFASTKD1 vector (C) and in HCMECs transfected with the sh-NC or sh-circFASTKD1 vector (D). (E, F) The cell growth curves of HUVECs (E) and HCMECs (F) transfected with the indicated vectors were determined using a CCK-8 assay. (G, H) The effects of transfection with the indicated vectors on the tube formation abilities of HUVECs (G) and HCMECs (H). (I, J) Transwell chambers were used to perform cell migration assays in HUVECs (I) or HCMECs (J) transfected with the indicated vectors. (K, L) Wound healing assays were used to examine the motility of HUVECs (K) and HCMECs (L) transfected with the indicated vectors. Data are presented as the mean of three experiments, and the error bars represent the SD (*P<0.05 and **P<0.01).