中华心血管病杂志
中華心血管病雜誌
중화심혈관병잡지
Chinese Journal of Cardiology
2012年
7期
601-606
,共6页
楚玉峰%陈闻东%蒋进皎%孟玫%曾娟%王春亭%高平进
楚玉峰%陳聞東%蔣進皎%孟玫%曾娟%王春亭%高平進
초옥봉%진문동%장진교%맹매%증연%왕춘정%고평진
GTP结合蛋白质类%血管内膜%转染
GTP結閤蛋白質類%血管內膜%轉染
GTP결합단백질류%혈관내막%전염
GTP-binding proteins%Tunica intima%Transfection
目的 探讨小分子G蛋白RhoA在大鼠颈动脉球囊损伤后新生内膜形成中的作用和相关机制.方法 将3～4月龄健康雄性SD大鼠分为5组:A组为正常对照组(10只)；B组为颈动脉球囊损伤组(10只)；C组为颈动脉球囊损伤+Ad-CMV-eGFP+ Pluronic F-127生物胶组(10只)；D组为颈动脉球囊损伤+ Ad-CMV-N19RhoA-eGFP组+Pluronic F-127生物胶(10只)；E组为颈动脉未损伤+ Ad-CMV-eGFP+ Pluronic F-127生物胶组(10只).建立颈动脉球囊损伤大鼠模型后,经血管外膜途径局部转染表达目的基因N19RhoA的重组腺病毒,分析其对损伤血管新生内膜增生及组织中细胞增殖核抗原和α平滑肌细胞肌动蛋白表达的影响.结果 大鼠颈动脉球囊损伤后14 d,B组RhoA蛋白表达量高于A组(P＜0.01).免疫组织化学检查显示,血管组织中细胞增殖核抗原和α平滑肌细胞肌动蛋白的阳性细胞率C组分别为45.2％和75.6％,D组分别为28.4％和51.9％,两组间差异均有统计学意义(P均＜0.01).D组血管新生内膜面积小于C组[(0.14±0.08) mm2比(0.23±0.10)mm2,P＜0.01],管腔面积大于C组[(0.47±0.11) mm2比(0.31±0.06) mm2,P＜0.01].结论 基因转染N19RhoA可抑制颈动脉球囊损伤后局部新生内膜形成,该作用可能与RhoA参与血管外膜成纤维细胞的增殖、表型转化以及迁移有关.
目的 探討小分子G蛋白RhoA在大鼠頸動脈毬囊損傷後新生內膜形成中的作用和相關機製.方法 將3～4月齡健康雄性SD大鼠分為5組:A組為正常對照組(10隻)；B組為頸動脈毬囊損傷組(10隻)；C組為頸動脈毬囊損傷+Ad-CMV-eGFP+ Pluronic F-127生物膠組(10隻)；D組為頸動脈毬囊損傷+ Ad-CMV-N19RhoA-eGFP組+Pluronic F-127生物膠(10隻)；E組為頸動脈未損傷+ Ad-CMV-eGFP+ Pluronic F-127生物膠組(10隻).建立頸動脈毬囊損傷大鼠模型後,經血管外膜途徑跼部轉染錶達目的基因N19RhoA的重組腺病毒,分析其對損傷血管新生內膜增生及組織中細胞增殖覈抗原和α平滑肌細胞肌動蛋白錶達的影響.結果 大鼠頸動脈毬囊損傷後14 d,B組RhoA蛋白錶達量高于A組(P＜0.01).免疫組織化學檢查顯示,血管組織中細胞增殖覈抗原和α平滑肌細胞肌動蛋白的暘性細胞率C組分彆為45.2％和75.6％,D組分彆為28.4％和51.9％,兩組間差異均有統計學意義(P均＜0.01).D組血管新生內膜麵積小于C組[(0.14±0.08) mm2比(0.23±0.10)mm2,P＜0.01],管腔麵積大于C組[(0.47±0.11) mm2比(0.31±0.06) mm2,P＜0.01].結論 基因轉染N19RhoA可抑製頸動脈毬囊損傷後跼部新生內膜形成,該作用可能與RhoA參與血管外膜成纖維細胞的增殖、錶型轉化以及遷移有關.
목적 탐토소분자G단백RhoA재대서경동맥구낭손상후신생내막형성중적작용화상관궤제.방법 장3～4월령건강웅성SD대서분위5조:A조위정상대조조(10지)；B조위경동맥구낭손상조(10지)；C조위경동맥구낭손상+Ad-CMV-eGFP+ Pluronic F-127생물효조(10지)；D조위경동맥구낭손상+ Ad-CMV-N19RhoA-eGFP조+Pluronic F-127생물효(10지)；E조위경동맥미손상+ Ad-CMV-eGFP+ Pluronic F-127생물효조(10지).건립경동맥구낭손상대서모형후,경혈관외막도경국부전염표체목적기인N19RhoA적중조선병독,분석기대손상혈관신생내막증생급조직중세포증식핵항원화α평활기세포기동단백표체적영향.결과 대서경동맥구낭손상후14 d,B조RhoA단백표체량고우A조(P＜0.01).면역조직화학검사현시,혈관조직중세포증식핵항원화α평활기세포기동단백적양성세포솔C조분별위45.2％화75.6％,D조분별위28.4％화51.9％,량조간차이균유통계학의의(P균＜0.01).D조혈관신생내막면적소우C조[(0.14±0.08) mm2비(0.23±0.10)mm2,P＜0.01],관강면적대우C조[(0.47±0.11) mm2비(0.31±0.06) mm2,P＜0.01].결론 기인전염N19RhoA가억제경동맥구낭손상후국부신생내막형성,해작용가능여RhoA삼여혈관외막성섬유세포적증식、표형전화이급천이유관.
Objective To investigate the role of small G-protein RhoA in neointimal formation following rat carotid artery balloon injury and related mechanisms.Methods Male 3-4-month-old SpragueDawley rats were used in the present study ( 10 rats per group).Group A:control; Group B:carotid artery balloon injury; Group C:injury + Ad-CMV-eGFP + Pluronic F-127; Group D:injury + Ad-CMV-N19RhoA -eGFP + Pluronic F-127 ; Group E:non injury + Ad-CMV-eGFP + Pluronic F-127.Perivascular gene transfer of an adenovirus co-expressing N19RhoA was performed to rat carotid artery following balloon injury and the effect on neointimal formation and the expressions of PCNA and α-SM-actin examined.Rats were killed after 14 days.Results The protein expression of RhoA in group B was significantly higher than in group A ( P =0.001 ),and the positive cells rate of PCNA and α-SM-actin which were assessed by immunohistochemistry in group C (45.2％ and 75.6％ ) was significantly higher than in group D ( 28.4％and 51.9％,all P ＜ 0.01 ).The area of neointima was significantly smaller [ (0.14 ± 0.08) mm2 vs.(0.23 ± 0.10) mm2,P ＜ 0.01 ],the luminal area was significantly larger [ (0.47 ± 0.11 ) mm2 vs.(0.31 ±0.06) mm2,P ＜ 0.01 ] in group D than in group C.Conclusion Gene transfer of N19RhoA attenuates neointimal formation after balloon injury in rat carotid arteries possibly related to the modulating capacities of small G-protein RhoA on the proliferation,phenotypic differentiation and migration of vascular adventitial fibroblasts.
