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

被引:14
|
作者
Yao, Qing-Ping [1 ]
Liu, Ze [1 ]
Yao, Ai-Hong [2 ]
Liu, Ji-Ting [1 ]
Jiang, Jun [3 ]
Chen, Yi [1 ]
Li, Shan-Shan [1 ]
Han, Yue [1 ]
Jiang, Zong-Lai [1 ]
Qi, Ying-Xin [1 ]
机构
[1] Shanghai Jiao Tong Univ, Sch Life Sci & Biotechnol, Inst Mechanobiol & Med Engn, 800 Dongchuan Rd, Shanghai 200240, Peoples R China
[2] Harbin Engn Univ, Coll Comp Sci & Technol, Inst Embedded Comp & IoT, Harbin, Peoples R China
[3] Southwest Med Univ, Affiliated Hosp, Dept Surg, Luzhou, Peoples R China
基金
中国国家自然科学基金;
关键词
circular RNAs; migration; miR-351-5p; vascular smooth muscle cells; vein graft; NEOINTIMAL HYPERPLASIA; MECHANICAL STRETCH; DISEASE; PROLIFERATION; PATHOGENESIS; PROTECTS; THERAPY; HEART;
D O I
10.1002/jcp.29577
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
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.
引用
收藏
页码:6831 / 6842
页数:12
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