Autologous vein graft stenosis inhibited by orphan nuclear receptor Nur77-targeted siRNA.
Neointimal hyperplasia plays an important role in autologous vein graft stenosis, and orphan receptor TR3/nur77 (Nur77) might play an essential role, but the mechanisms are still unclear. Here, we investigated the function of Nur77 in autologous vein graft stenosis. Rat vascular smooth muscle cell A7r5 was used for evaluating the function of Nur77 and screen siRNAs. Meanwhile, rat vein graft models were constructed for investigating the stenosis inhibition effects of Nur77-targeted siRNAs. The mRNA and protein levels of Nur77 were highly expressed in A7r5 cell, and could be significantly inhibited by the pre-designed siRNAs; the proliferation of A7r5 cell was also inhibited by the siRNAs. Furthermore, the intimal thickening in rat vein graft models was inhibited when knocking down the expression of Nur77 by siRNA. The results suggest that Nur77-targeted siRNA can inhibit autologous vein graft stenosis, Nur77 may play an important role in autologous vein graft stenosis, and Nur77 targeted siRNAs may be a therapy method for anti-stenosis of autologous vein graft.
Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Kun
K
Liu
Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China.
Wen
W
Zhou
Nantong University, Nantong 226001, China.
Honglin
H
Chen
Department of Cardiology, Affiliated Hospital of Nantong University, Nantong 226001, China.
Haiyan
H
Pan
Department of Cardiology, Nantong Geriatric Rehabilitation Hosptial, Nantong 226001, China.
Xiaohui
X
Sun
Department of Cardiothoracic Surgery, Affiliated Hospital of Nantong University, Nantong 226001, China. Electronic address: litiejun0323@163.com.
Qingsheng
Q
You
D000818:Animals; D002339:Carotid Arteries / Q000601:surgery; D002460:Cell Line; D049109:Cell Proliferation; D004195:Disease Models, Animal; D006083:Graft Occlusion, Vascular / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D006801:Humans; D006965:Hyperplasia; D007601:Jugular Veins / Q000378:metabolism / Q000473:pathology / Q000637:transplantation*; D009131:Muscle, Smooth, Vascular / Q000378:metabolism* / Q000473:pathology; D032389:Myocytes, Smooth Muscle / Q000378:metabolism / Q000473:pathology; D058426:Neointima; D057105:Nuclear Receptor Subfamily 4, Group A, Member 1 / Q000235:genetics / Q000378:metabolism*; D034622:RNA Interference; D034741:RNA, Small Interfering / Q000235:genetics / Q000378:metabolism*; D000067492:RNAi Therapeutics; D017207:Rats, Sprague-Dawley; D015398:Signal Transduction; D013997:Time Factors; D014162:Transfection; D014182:Transplantation, Autologous
C539820:Nr4a1 protein, rat; D057105:Nuclear Receptor Subfamily 4, Group A, Member 1; D034741:RNA, Small Interfering
Nur77; Proliferation; RNA interfering; Vascular smooth muscle cell; Vein graft restenosis