Related Experiment Video
Updated: Apr 5, 2026
A Murine Model of Stent Implantation in the Carotid Artery for the Study of Restenosis
Published on: May 14, 2013
Tissue Factor Pathway Inhibitor-Coated Stents Inhibit Restenosis in a Rabbit Carotid Artery Model
Mingyu Shi1, Feng Yin1, Hongyue Gu1
1Department of Cardiovasology, The First Affiliated Hospital of Harbin Medical University, Harbin, China.
Introduction:
Our aim was to study the efficacy and safety of tissue factor pathway inhibitor (TFPI)-coated stents in inhibiting restenosis in a rabbit carotid artery model.
Methods:
Subculture was conducted in aorta smooth muscle cell, which was taken from male Wistar rat, and the 3-5-generation cells were taken for plasmid transfection and cytotoxicity experiment. TFPI microspheres were made of a TFPI plasmid which was enwrapped by poly-l-glutamic acid (PLGA). TFPI-coated stents (n = 7) and bare metal stents (n = 6) were implanted into prepared carotid artery stenosis model of New Zealand white rabbits. The transfection efficiency of TFPI gene and its influence on animal tissue, restenosis inhibition, and biochemical indicator were observed.
Result:
Tissue factor pathway inhibitor microspheres can transfect successfully into cells, and present no cytotoxicity. Autopsy results showed no pathological changes in liver and spleen of rabbits after implanting TFPI-coated stents. TFPI gene could transfect and express successfully in vessel wall cells, and thrombus was found in some lumens of bare metal stents group after 7 day, while no such thrombus was observed in coated stents group. Degree of hyperplasia of coronary endarterectomy in bare metal stents group was evidently higher than those in coated stents group. Obvious stent restenosis was discovered only in one case in bare metal stents group (diameter stenosis ≥50%). However, no case in coated stents group showed with stent restenosis.
Conclusion:
Tissue factor pathway inhibitor-coated stents could successfully transfect TFPI gene into vessel wall cells, thereby inhibiting restenosis without obvious side effect in the rabbit carotid artery model.
Insights
Tissue factor pathway inhibitor (TFPI)-coated stents successfully inhibited restenosis in rabbits by delivering TFPI gene to vessel walls. This novel approach shows promise for preventing artery narrowing without significant side effects.
Area of Science:
- Biomedical Engineering
- Vascular Biology
- Gene Therapy
Background:
- Restenosis remains a significant complication after vascular interventions.
- Tissue factor pathway inhibitor (TFPI) plays a crucial role in regulating coagulation and inflammation.
- Developing effective strategies to prevent restenosis is a key challenge in cardiovascular medicine.
Purpose of the Study:
- To evaluate the efficacy and safety of TFPI-coated stents in preventing restenosis.
- To assess the gene transfection efficiency and expression of TFPI in vessel wall cells.
- To investigate the impact of TFPI-coated stents on neointimal hyperplasia and thrombus formation.
Main Methods:
- TFPI microspheres were prepared using PLGA and a TFPI plasmid.
- TFPI-coated stents and bare metal stents were implanted in a rabbit carotid artery stenosis model.
- Transfection efficiency, cytotoxicity, pathological changes, restenosis inhibition, and biochemical indicators were assessed.
Main Results:
- TFPI microspheres demonstrated successful cellular transfection with no cytotoxicity.
- TFPI gene successfully transfected and expressed in vessel wall cells, with no adverse effects on rabbit liver or spleen.
- TFPI-coated stents significantly reduced neointimal hyperplasia and prevented thrombus formation compared to bare metal stents.
- No stent restenosis was observed in the TFPI-coated stent group, while one case occurred in the bare metal stent group.
Conclusions:
- TFPI-coated stents effectively deliver TFPI gene to vessel wall cells.
- TFPI-coated stents demonstrate significant efficacy in inhibiting restenosis in a rabbit carotid artery model.
- The TFPI-coated stent approach appears safe, with no observed side effects.
