文章摘要
郝广华 汪南平 黄雅姿 赵蓓蕾 张弘.视黄醇结合蛋白4 对血管平滑肌细胞迁移和增殖的影响及机制[J].,2016,16(17):3212-3216
视黄醇结合蛋白4 对血管平滑肌细胞迁移和增殖的影响及机制
Role of RBP4 in Vascular Smooth Muscle Cells Migration and Proliferationand Its Molecular Mechanism
  
DOI:
中文关键词: 视黄醇结合蛋白  动脉粥样硬化  平滑肌细胞  迁移  增殖
英文关键词: Retinol binding protein  Atherosclerosis  Smooth muscle cell  Migration  Proliferation
基金项目:国家自然科学基金项目(30900693);中国博士后科学基金会基金项目(20080440284)
作者单位
郝广华 汪南平 黄雅姿 赵蓓蕾 张弘 西安交通大学医学院第二附属医院心内科北京大学心血管研究所分子心血管学教育部重点实验室 
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中文摘要:
      目的:研究视黄醇结合蛋白4(Retinol-binding protein 4,RBP4)对血管平滑肌细胞(SMCs)迁移和增殖的影响及分子机制。方 法:体外培养大鼠主动脉SMCs,采用划痕实验及Boyden's 迁移小室实验观察RBP4 对SMCs 迁移的影响,采用免疫印迹实验技 术检测Akt 的磷酸化水平,采用Boyden's 小室实验观察PI3K 抑制剂LY294002 预处理细胞对RBP4 促SMCs 迁移的影响,应用 MTT 比色实验结合流式细胞仪技术,检测RBP4 对SMCs 细胞增殖及细胞周期的影响。结果:RBP4 呈剂量依赖性诱导大鼠血管 SMCs迁移(P<0.05);RBP4 处理细胞显著增加了Akt 磷酸化;PI3K 抑制剂LY294002 预处理细胞则显著抑制了RBP4的促迁移 作用(P<0.05);RBP4 处理有增加SMCs数量的趋势,且可轻微阻滞细胞进入S期,但未达到统计学显著性(P>0.05)。结论:RBP4 通过PI3K-Akt通路诱导大鼠血管SMCs迁移,对细胞增殖及细胞周期则无显著影响。
英文摘要:
      Objective:To explore a potential role of retinol-binding protein 4 (RBP4) in vascular smooth muscle cells (SMCs) migration and proliferation and its molecular mechanism.Methods:Vascular SMCs of rat were cultured in vitro. Vascular SMCs migration was studied by scratch assay and Boyden's chamber. Western blot analysis was used for detecting Akt and phospho-Akt protein levels. SMCs were pretreated with PI3K inhibitor LY294002, Boyden's chamber was then used for detecting RBP4-induced cell migration. Cell proliferation and cell cycle of vascular SMCs induced by RBP4 was detected by use of MTT dye absorbance and flow cytometry.Results:Recombinant human RBP4 significantly induced migration of rat vascular SMCs in a dose-dependent fashion (P<0.05) and phosphorylation of Akt at the same time. PI3K inhibitor Ly294002 significantly suppressed RBP4's effects on cell migration (P<0.05). RBP4 treatment slightly increased SMCs proliferation and led to G1/S cell cycle arrest, but these effects did not reach statistical significance.Conclusion:RBP4 induces migration of vascular SMCs through PI3K-Akt-dependent pathways. However, the proliferation and cell cycle progression of the SMCs is not affected by RBP4 treatment.
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