| Krüppel样因子5介导血管平滑肌细胞的增殖和迁移 |
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| 引用本文： | 刘玉,王海军,李爱英,李楠,韩梅.Krüppel样因子5介导血管平滑肌细胞的增殖和迁移[J].细胞生物学杂志,2012(11):1095-1100. |
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| 作者姓名： | 刘玉 王海军 李爱英 李楠 韩梅 |
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| 作者单位： | [1]河北医科大学基础医学院生物化学教研室,石家庄050017 [2]河北医科大学中医学院生物化学教研室,河北省医学生物技术重点实验室,石家庄050091 [3]河北大学附属医院普通外科,保定071000 |
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| 基金项目： | 国家自然科学基金（No.31071003）; 河北省自然科学基金（No.C2009001053）; 河北省教育厅（No.2010262）资助项目 |
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| 摘 要： | Krüppel样因子5（krüppel-like factor 5,KLF5）是KLF家族中与胚胎发育、细胞增殖和肿瘤发生密切相关的转录调节因子。为观察KLF5在体外培养的大鼠血管平滑肌细胞（vascularsmooth muscle cells,VSMCs）增殖和迁移活性中的作用,通过构建KLF5腺病毒表达载体并感染细胞以过表达KLF5或用特异性siRNA敲低KLF5,用MTT、流式细胞术以及免疫细胞化学染色和伤口愈合实验检测其对VSMCs增殖和迁移活性的影响。结果发现,KLF5过表达可加速细胞由G0/G1期向S期转变,促进细胞增殖和迁移;反之,敲低KLF5后细胞增殖活性明显低于转染无关序列NS-siRNA对照组细胞,G0/G1期细胞数所占比例增多,S期细胞数所占比例减少,VSMCs迁移活性也明显降低。结果表明KLF5可参与介导VSMCs的增殖和迁移。
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| 关 键 词： | Krüppel样因子5 增殖 迁移 血管平滑肌细胞 |
Krüppel-like Factor 5 Promotes VSMC Proliferation and Migration |
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| Liu Yu,Wang Haijun,Li Aiying,Li Nan,Han Mei.Krüppel-like Factor 5 Promotes VSMC Proliferation and Migration[J].Chinese Journal of Cell Biology,2012(11):1095-1100. |
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| Authors: | Liu Yu Wang Haijun Li Aiying Li Nan Han Mei |
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| Institution: | 1The Key Laboratory of Medical Biotechnology of Hebei, Department of Biochemistry, Institute of Basic Medicine, Hebei Medical Unibersity, Shijiazhuang 050017, China; 2Department of Biochemistry, Traditional Chinese Medical College, Hebei Medical University, Shijiazhuang 050091, China; 3Department of General Surgery, Hebei University, Baoding 071000, China) |
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| Abstract: | Krüppel-like factor 5 （KLF5）, a member of the Sp/KLF family of zinc finger factors, is a key regulator of cardiovascular remodeling. To determine the role of KLF5 in cell proliferation and migration, VSMCs were infected with Ad-KLF5 to over-express KLF5, and transfected KLF5-specific siRNA to knockdown the en-dogenous KLF5, respectively. The activity of the cell proliferation and migration was detected using MTT assay, flow cytometric analysis, immunocytochemistry and wound healing assays, respectively. The results showed that the over-expression of KLF5 increased the expression of PCNA protein in VSMCs, and resulted in an increase in proliferation and number of S-phase cells, compared with empty vector controls. In addition, the migration activity increased in KLF5-overexpressed VSMC. Conversely, the knockdown of KLF5 by specific siRNA abolished Ang Ⅱ-induced cell growth via reduction of the number of S-phase cells, inhibited the migration of VSMCs. These find- ings indicate that KLF5 is required for VSMC proliferation and migration. |
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| Keywords: | KLF5 proliferation migration VSMC |
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