Circular RNA circTET3 mediates migration of rat vascular smooth muscle cells by targeting miR‐351‐5p

Abnormal migration and proliferation of vascular smooth muscle cells (VSMCs) are the pathological basis of hyperplasia during vein graft disease. It remains unknown if circular RNAs (circRNAs) are involved in vein graft disease. In the present study, a rat vein graft model was constructed by the “cuff” technique, and whole transcriptome deep sequencing was applied to identify differential circRNAs in the grafted vein compared to the control. We identified a novel circRNA, named circTET3, whose structure was verified by Sanger sequencing and RNase R digestion. CircTET3 was increased in the grafted vein and stably located in the cytoplasm as detected by fluorescence in situ hybridization. Knockdown of circTET3 suppressed VSMC migration by acting as an endogenous miR‐351‐5p sponge detected by RNA pull‐down and dual‐luciferase reporter assays. PTPN1 was the targeted gene due to the competitive binding of circTET3 to miR‐351‐5p. This regulatory pathway may serve as a potential therapeutic avenue against intimal hyperplasia in vein graft disease. CircTET3, which was transcribed from the 4th exon of tet3 and stably located in the cytoplasm, was increased in the grafted vein compared to the control vein. CircTET3 suppressed vascular smooth muscle cells migration by acting as an endogenous miR‐351‐5p sponge. PTPN1 was the targeted gene due to the competitive binding of circTET3 to miR‐351‐5p.