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flk-1基因在胎肝造血细胞增殖中的调控作用 被引量:1

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摘要 【目的】探讨flk-1基因在胎肝造血细胞体外扩增中的调控作用。【方法】体外培养E14胎肝造血细胞,应用Western-Blot检测flk-1配基VEGF及其抑制剂SU5416对E14胎肝造血细胞flk-1蛋白表达水平的影响,通过细胞计数、氚标胸腺嘧啶脱氧核苷掺入实验及细胞周期分析观察flk-1配基VEGF及其抑制剂SU5416对E14胎肝造血细胞增殖的影响,造血集落CFU-GM(colony-forming unit-granulocyte/macrophage粒-巨噬细胞系集落形成单位)培养检测造血祖细胞的功能状态。【结果】VEGF或VEGF加SU5416均可促进胎肝造血细胞的增殖,细胞数目分别为对照组的108%和142%,并且集落数量也显著增加,分别为对照组的159%和151%(P<0.01);单独应用SU5416使造血细胞的数目较对照组减少了8%,但集落产率与对照组无显著性差异。Western blot结果经统计学分析,SU5416组和VEGF加SU5416组flk-1蛋白表达强度分别为对照组的165%(P<0.01)和57%(P<0.05),与对照组相比有显著性差异。【结论】VEGF受体flk-1和flt-1均参与介导VEGF对胎肝造血细胞增殖的调控作用。SU5416阻断flk-1信号转导可上调flk-1的蛋白表达,Flt-1活化可下调flk-1的蛋白表达。
出处 《中山大学学报(医学科学版)》 CAS CSCD 北大核心 2009年第A03期1-4,共4页 Journal of Sun Yat-Sen University:Medical Sciences
基金 国家自然科学基金(No.30400225) 广东省自然科学基金(No.04300227)
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共引文献23

同被引文献8

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