我们的网站为什么显示成这样？

可能因为您的浏览器不支持样式，您可以更新您的浏览器到最新版本，以获取对此功能的支持，访问下面的网站，获取关于浏览器的信息：

|本期目录/Table of Contents|

曲古菌素A抑制血管平滑肌细胞增殖和迁移的研究(PDF)

《心脏杂志》[ISSN:1009-7236/CN:61-1268/R]

期数:
2008年第3期
页码:
295-300
栏目:
基础研究
出版日期:
2008-05-20

文章信息/Info

Title:
Effect of Trichostatin A on proliferation and migration of vascular smooth muscle cells
作者:
邹琛; 徐志红; 吴春芳; 陆国平
上海交通大学附属瑞金医院心脏科，上海 200025
Author(s):
ZOU Chen;  XU ZhiHong;  WU ChunFang;  LU Guoping
Department of Cardiology, RuiJin Hospital, Shanghai Jiaotong University, Shanghai 200025, China
关键词:
曲古菌素A; 血管平滑肌; 细胞周期; 凋亡
Keywords:
trichostatin A;  vascular smooth muscle cell;  cell cycle;  apoptosis
分类号:
R979.1
DOI:
-
文献标识码:
A
摘要:
目的 观察曲古菌素A(trichostatin A,TSA)体外抑制血管平滑肌细胞（VSMCs）增殖、迁移和诱导凋亡的作用。方法 采用MTT比色法和BrdU掺入法，观察TSA对胎牛血清诱导的VSMCs增殖的抑制作用。采用流式细胞术和Western blot检测细胞周期蛋白的表达，观察TSA对VSMC细胞周期的影响。采用ELISA法测定DNA片段和Western blot检测活化caspase3的表达，观察TSA诱导VSMC发生凋亡的作用。结果 100 μg/L TSA可抑制胎牛血清诱导的VSMC增殖而无明显的细胞毒作用，1 000 μg/L TSA可激活caspase3并诱导VSMC发生凋亡。TSA干预可延缓胎牛血清诱导的VSMC进入S期，此效应与抑制周期蛋白cyclin D1和周期蛋白cyclin A的表达有关。TSA能抑制胎牛血清诱导的张力纤维Factin解聚和重组，抑制VSMC迁移。结论 TSA能抑制胎牛血清诱导的VSMC增殖，使之停滞于静止期，大剂量TSA可诱导VSMC凋亡，并能抑制VSMC迁移。因此，TSA有望成为治疗血管增殖性疾病的一种新策略。
Abstract:
AIM To study the effect of Trichostatin A (TSA) on vascular smooth muscle cells (VSMCs) proliferation, migration and apoptosis in vitro. METHODS VSMCs proliferation was analyzed by MTT colormetry and BrdU incorporation assay. Cellular cycle phase distributions were determined by flow cytometry. The expression of cyclin D1 and cyclin A was assessed by Western blot and cell apoptosis was quantified by detecting cytoplasmic histoneassociated DNAfragments and the level of cleaved caspase3. RESULTS 100 μg/L TSA inhibited fetal bovine serum (FBS)induced VSMC proliferation with no significant cytotoxity. 1 000 μg/L TSA activated caspase3 and induced VSMC apoptosis. TSA treatment suppressed expression of cyclin D1 and cyclin A and blocked VSMCs to enter S phase. TSA blocked FBSinduced Factin depolymerization, recombination and inhibited VSMC migration. CONCLUSION TSA inhibits FBSinduced VSMC proliferation and migration. High dose of TSA induces VSMC apoptosis. TSA may provide a novel therapy for vascular proliferative diseases.

参考文献/References

［1］ Costa MA, Simon DI. Molecular basis of restenosis and drugeluting stents[J]. Circulation, 2005, 111(17):2257-2273.

[2] Andres V, Castro C. Antiproliferative strategies for the treatment of vascular proliferative disease[J]. Curr Vasc Pharmacol, 2003, 1(1):85-98.

[3] Marks P, Rifkind RA, Richon VM, et al. Histone deacetylases and cancer: causes and therapies[J]. Nat Rev Cancer, 2001, 1(3):194-202.

[4] Bolden JE, Peart MJ, Johnstone RW. Anticancer activities of histone deacetylase inhibitors[J]. Nat Rev Drug Discov, 2006, 5(9):769-784.

[5] Sarkar R, Meinberg EG, Stanley JC, et al. Nitric oxide reversibly inhibits the migration of cultured vascular smooth muscle cells[J]. Circ Res, 1996, 78(2):225-230.

[6] Monneret C. Histone deacetylase inhibitors[J]. Eur J Med Chem, 2005, 40(1):1-13.

[7] Ranganna K, Joshi T, Yatsu FM. Sodium butyrate inhibits plateletderived growth factorinduced proliferation of vascular smooth muscle cells[J]. Arterioscler Thromb Vasc Biol, 1995, 15(12):2273-2283.

[8] Okamoto H, Fujioka Y, Takahashi A, et al. Trichostatin A, an inhibitor of histone deacetylase, inhibits smooth muscle cell proliferation via induction of p21(WAF1)[J]. J Atheroscler Thromb, 2006, 13(4):183-191.

备注/Memo

备注/Memo:
收稿日期：2007-06-27.通讯作者：陆国平，教授，主任医师，主要从事血管增殖性疾病的分子治疗的研究Email：gplu52@hotmail.com 作者简介：邹琛，主治医师，博士生 Email:zouchen621@hotmail.com
更新日期/Last Update: