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血管紧张素II型受体基因转染表达对血管平滑肌细胞迁移的影响(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2001年第5期
页码:
348-351
栏目:
论著
出版日期:
2001-09-01

文章信息/Info

Title:
Expression of transferred angiotens in II type 2 receptor gene inhibits the migration of vascular smooth muscle cells in vitro
作者:
刘建平;  何国祥;  景　涛;  王　旭;  史光鉴
第三军医大学西南医院心内科, 重庆400038
Author(s):
LIU Jian-ping ;  HE Guo-xiang ;  JING Tao; WANG Xu;  SHI Guang-jian
Department of Cardiology, Southwest Hospital, Third Military Medical University, Chongqing400038, China
关键词:
受体;  血管紧张素;  腺病毒载体;  迁移;  血管平滑肌细胞
Keywords:
receptor;  angiotensin;  adenovirus vector; migration;  vascular smooth muscle cell
分类号:
Q342.3
DOI:
-
文献标识码:
A
摘要:
目的 探讨血管紧张素II(AngII ) 2 型受体(AT2R) 基因表达对血管平滑肌细胞(VSMC) 迁移能力的影响。方法 构建带AT2R 基因的重组复制缺陷腺病毒载体(AdCMV-AT2R) , 体外转染培养的大鼠主动脉VSMC, 用流式细胞仪检测AT2R 转染表达率, RT-PCR 方法检测AT2R mRNA 表达,VSMC 迁移用改良Boyden’s 趋化小室法检测, 用激光共聚焦显微镜检测细胞骨架蛋白F-actin 的表达。结果 构建的AdCMV-AT2R 体外转染培养VSMC表达率为89. 5%。AT2R 峰值表达时,VSMC 的跨膜迁移数降低62.2% , F-actin 表达明显减少。结论 AT2R 转染表达可显著抑制体外培养VSMC 迁移, 这为防治血管再狭窄提供了新的思路。
Abstract:
AIM To study the expression of angiotensin II (AngII ) type 2 receptor (AT2R ) and its effect on the migration of vascular smooth muscle cell (VSMC ) in rats. METHODS The recombinant adenoviral vector,AdCMV-AT2R, containing rat AT2 receptor gene was constracted by homologous recombination, and then it was used to transfer AT2 receptor gene to rat VSMC in vitro. The expression of AT2R mRNA was detected by RT-2PCR and the rate of expression in VSMC was determined by flow cytometer. The modified Boyden’s chamber method was used to test the migration of VSMC. The reorganization of Factin in VSMC was analysed by confocal microscopy. RESULTS RT-PCR showed that the expression of AT2R mRNA increased obviously in transferred VSMC, and the peak value of expression rate is about 89. 5% at 48 h.When the expression of AT2R is at peak value, the number of VSMC migration was reduced by 62. 2% (P < 0. 05) and the expression of F2act in was also decreased obviously. CONCLUSION AdCMV-AT2R can generate high level expression of AT2 receptor in cultured rat VSMC. The adenovirus-mediated expression of AT2 receptor can significantly inhibit the migration of rat VSMC in vitro. It may be a new selection for the gene therapy of restenosis after angioplasty.

参考文献/References

[1] Nikol S, Huehns TY, Hoffling B. Molecular biology and post angioplasty restenosis[J]. Atherosclerosis, 1996, 123: 17- 31.

[2]Matsubara H. Pathophysiological role of angiotensin II type 2 receptor in cardiovascular and renal diseases [J]. Circ Res,1998, 83: 1182.

[3] Horiuchi M , Akishita M , Dzau VJ. Recent progress in angiotensin II type 2 receptor research in the cardiovascular system [J]. Hypertension, 1999, 33: 613- 621.

[4] Sugawara Y, Sakata Y,Minowada S, et al. Adenovirus-mediated transfer of tissue-type plasminogen activator gene to human endothelial cells[J]. Surgery , 1997, 122: 91- 100.

[5] Matrougui K, Loufrani L , Heymes C, et al. Activation of AT2 recetors by endogenous angiotensin II is involved in flow-induced dilation in rat resistance arteries [J]. Hypertension,1999, 34: 659- 665.

[6] Nozawa Y,Matsuura N ,Miyake H, et al. Effects of TH142177on angiotensin II-induced proliferation, migration and intracellular signaling in vascular smooth muscle cells and on neointimal thickening after balloon injury [J]. Life Science,1999, 64: 2061- 2070.

[7] Ishida T, Ishida M , Suero J , et al. Agonist-stimulated cytoskeletal reorganization and signal transductin at focal adhesions in vascular smooth muscle cells requrie c-Src [J]. J Clin Invest, 1999, 103 (6) : 789- 797.

[8] Casscells W. Migration of smooth muscle and endothelial cells.Critical events in restenosis [J]. Circulation, 1992, 86: 723 -729.

[9] Sheetz MP, Felsenfeld D, Galbraith CG, et al. Cell migration as a vive-step cycle[J]. Biochem Soc Symp , 1999, 65: 233- 243.

备注/Memo

备注/Memo:
收稿日期：2000-09-29.
更新日期/Last Update: 2001-09-01