神经损伤与功能重建
神經損傷與功能重建
신경손상여공능중건
NEURAL INJURY AND FUNCTIONAL RECONSTRUCTION
2014年
3期
187-190
,共4页
静亮%彭希%谢敏杰%喻志源%吕家高%王伟
靜亮%彭希%謝敏傑%喻誌源%呂傢高%王偉
정량%팽희%사민걸%유지원%려가고%왕위
支架术后再狭窄%药物洗脱支架%重组慢病毒%细胞周期
支架術後再狹窄%藥物洗脫支架%重組慢病毒%細胞週期
지가술후재협착%약물세탈지가%중조만병독%세포주기
in-stent restenosis%drug-eluting stents%recombinant lentivirus%cell cycle
目的：构建由 SM22α特异性启动子介导血管平滑肌细胞（VSMCs）靶向性过表达 p27蛋白的慢病毒载体来研究对 VSMCs 细胞周期的影响。方法：构建重组慢病毒载体（Lenti-SM22α-p27-EGFP），感染原代培养的 VSMCs 及内皮细胞（VECs）。结果：SM22α-p27慢病毒能对 VSMCs 表现出高效且精确的抑制作用。SM22α启动子靶向标记的 p27能在 VSMCs 内过表达，且通过 G0/G1期阻滞来抑制细胞增殖。结论：由SM22α特异性启动子驱动的重组慢病毒载体能选择性感染 VSMCs，有效地引起 p27蛋白过表达并产生G0/G1期阻滞。
目的：構建由 SM22α特異性啟動子介導血管平滑肌細胞（VSMCs）靶嚮性過錶達 p27蛋白的慢病毒載體來研究對 VSMCs 細胞週期的影響。方法：構建重組慢病毒載體（Lenti-SM22α-p27-EGFP），感染原代培養的 VSMCs 及內皮細胞（VECs）。結果：SM22α-p27慢病毒能對 VSMCs 錶現齣高效且精確的抑製作用。SM22α啟動子靶嚮標記的 p27能在 VSMCs 內過錶達，且通過 G0/G1期阻滯來抑製細胞增殖。結論：由SM22α特異性啟動子驅動的重組慢病毒載體能選擇性感染 VSMCs，有效地引起 p27蛋白過錶達併產生G0/G1期阻滯。
목적：구건유 SM22α특이성계동자개도혈관평활기세포（VSMCs）파향성과표체 p27단백적만병독재체래연구대 VSMCs 세포주기적영향。방법：구건중조만병독재체（Lenti-SM22α-p27-EGFP），감염원대배양적 VSMCs 급내피세포（VECs）。결과：SM22α-p27만병독능대 VSMCs 표현출고효차정학적억제작용。SM22α계동자파향표기적 p27능재 VSMCs 내과표체，차통과 G0/G1기조체래억제세포증식。결론：유SM22α특이성계동자구동적중조만병독재체능선택성감염 VSMCs，유효지인기 p27단백과표체병산생G0/G1기조체。
ObjectiveTo construct Lenti-SM22alpha-p27-EGFP recombinant lentiviral vectors targeting vascular smooth muscle cells (VSMCs) and to investigate the impact on VSMCs proliferation by cell cycle analysis. Methods: Recombinant lentiviruses were constructed. The viruses were transfected into VSMCs and vascular endothelial cells (VECs). Results: SM22α-p27 lentiviruses exhibited effective and specific inhibition on VSMCs. SM22α promoter targeted p27 was able to be selectively over-expressed in VSMCs and to inhibit proliferation by cell cycle arrest at G0/G1. Conclusion: Recombinant lentiviruses driven by SM22α promoter could selectively infect VSMCs, thus lead to p27 protein over-expression and G0/G1 arrest.
