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骨髓间充质干细胞对K562细胞增殖及凋亡的影响 被引量:3

Effects of Human Bone Marrow Mesenchymal Stem Cells on Proliferation and Apoptosis of K562 Cells
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摘要 本研究比较K562细胞与相同数量以及不同数量的人骨髓间充质干细胞(MSC)黏附培养前后K562细胞增殖、细胞周期和凋亡的变化,以探讨MSC对人白血病K562细胞生长的影响。通过建立正常人骨髓MSC的体外培养体系及其与K562细胞共培养的体系测定K562细胞的生长曲线;将不同数量的MSC与K562细胞共培养测定K562细胞的增殖率曲线;应用流式细胞术检测K562细胞周期以及凋亡的变化。结果显示:与单独K562细胞培养相比,K562细胞与相同数量MSC共培养后,生长受抑;K562细胞与不同数量MSC共培养后,MSC对K562细胞的抗增殖作用呈剂量依赖性;细胞周期分析发现,K562细胞与MSC共培养后,G0/G1期以及G2/M期的细胞增加,S期的细胞减少。共培养24、48、72小时后流式细胞仪检测发现,K562细胞的凋亡率下降。结论:正常人骨髓MSC能使导致K562细胞生长抑制,阻止K562细胞周期的运行,凋亡率下降,且在一定范围内,随着MSC数量的增加,对K562细胞的抗增殖作用增强。 This study was aimed to compare K562 cell proliferation, cell cycle and apoptosis before and after adhesive culture with MSCs of the same and different counts, so as to investigate the effect of human bone marrow mesenchymal stem cells (MSCs) on the growth of K562 cells. Culture system of bone marrow MSCs and co-culture system of K562 cells and BMSCs in vitro were established. And K562 cell proliferation curves were drawn by co-cultured of K562 cells with different counts of BMSCs. Cell cycle and apoptosis were determined by flow cytometry. The results showed that compared with the control, the proliferation of K562 cells cultured with the same amounts of MSCs was inhibited. After co-culture with the different amounts of MSCs, MSCs exhibited a dose-dependent antiproliferation effect on K562 cells. The percentages of K562 cells in G1 phase and G2 phase were higher than those of the control. It is concluded that the normal bone marrow mesenchymal stem cells can inhibit the proliferation, the progress of cell cycle and the rate of apoptosis of K562 cells. As the number of mesenchymal stem cells increased, their antiproliferation effect on the K562 cells were enhanced in a certain range.
出处 《中国实验血液学杂志》 CAS CSCD 2009年第1期137-140,共4页 Journal of Experimental Hematology
基金 2007江苏省高校自然科学基础研究项目(编号07KJB320074) 国家自然科学基金资助项目(编号30500603) 江苏省2005年第二批省级产业技术研究与开发项目(编号20051125)
关键词 间充质干细胞 K562细胞 细胞增殖 细胞凋亡 mesenchymal stem cell K562 cell proliferation apoptosis
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参考文献9

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共引文献6

同被引文献29

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