phVEGF165 gene transfer for prevention of stent restenosis after TIPSS
- VernacularTitle:血管内皮细胞生长因子基因涂布支架预防门腔静脉分流支架狭窄的实验研究
- Author:
Zijun LI
;
Xiaoming CHENG
;
Pinjin HU
- Publication Type:Journal Article
- Keywords:
Trans-jugular intrahepatic portosystemic shunts;
Human vascular endothelial growth factor;
Stent;
Restenosis
- From:
Chinese Journal of Digestion
2001;0(01):-
- CountryChina
- Language:Chinese
-
Abstract:
Objective To test the hypothesis that locally direct gene transfer of human vascular endothelial growth factor(phVEGF) 165 could passivate hepatic venous metallic stents by accelerating endothelialization and augmenting biocompatibility of endovascular stent. Methods The complexes of pAdTrackCMV and lipofectamine was smeared homogeneously to the surface of stent coating with poly-1-lysine. Bare stainless steel stents were used as controls. All stents were implanted into the hepatic right vein by the procedure of transjugular intrahepatic venous stent deployment. Results At the end of 1 week after implantation, the site -specific expression of phVEGF was detected by RT-PCR. Green fluorescence and the expression of phVEGF gene were detected in the transfered stented vessel of the treatment group. These phenomena were not observed in the control group. Scanning electron microscopy revealed that the endothelialization of stent was more pronounced in the treatment group than that in control group. At the end of 8 weeks after implantation, quantitative angiography analysis showed the degree of internal diameter stenosis was less severe in the treatment group compared with the control group. Mean neointima thickness, mean neointima areas and percent cross-sectional area narrowing in treatment group was significantly fewer than that in the control group, respectively. Immunohistochemistry analysis revealed that the proliferation of vascular smooth muscle cells was more active in control group than that in the treatment group. Conclusions Local gene transfer of phVEGF165 can passivate endovascular stents by accelerating stents endothelization and enhancing their biocompatibility in hepatic vein, resulting in reducing thrombus formation and attenuating intimal hyperplasia.
