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Circular RNA circTET3 mediates migration of rat vascular smooth muscle cells by targeting miR‐351‐5p
Author(s) -
Yao QingPing,
Liu Ze,
Yao AiHong,
Liu JiTing,
Jiang Jun,
Chen Yi,
Li ShanShan,
Han Yue,
Jiang ZongLai,
Qi YingXin
Publication year - 2020
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.29577
Subject(s) - gene knockdown , vascular smooth muscle , in situ hybridization , biology , microbiology and biotechnology , circular rna , rna , microrna , rna interference , messenger rna , pathology , gene , medicine , biochemistry , smooth muscle , endocrinology
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.