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LAIR-1对巨核细胞系Dami生长分化的影响作用 被引量:1

Effects of LAIR-1 on the growth and differentiation of megakaryocytic cell line Dami
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摘要 研究LAIR-1在巨核细胞系Dami上的表达,及其表达对细胞生长分化的影响,为深入研究LAIR-1在巨核细胞造血中的功能奠定基础。采用流式细胞术和激光共聚焦显微镜检测LAIR-1分子的表达;应用CCK-8法、AnnexinV-FITC/PI双染流式细胞术检测LAIR-1对细胞增殖及凋亡的影响;应用PI染色流式细胞术检测LAIR-1对细胞倍性的影响。结果:LAIR-1在Dami细胞膜上低水平表达,PMA可以显著刺激其表达;应用特异性抗体或配体交联LAIR-1分子,与对照组相比,细胞的增殖降低、凋亡增多、分化过程中2N和4N的细胞较多、细胞上CD41a和CD42b的表达降低。提示,PMA可以显著诱导LAIR-1在Dami细胞上的膜表达;LAIR-1的表达抑制Dami细胞的增殖,刺激其凋亡,阻碍细胞核内DNA的复制,抑制细胞上CD41a和CD42b的表达。 To study the expression of LAIR-1 on the megakaryocytic cell line Dami,and the effect of its expression on the growth and differentiation of the cell line in order to lay a foundation for the deeper study in the function of LAIR-1 on the megakaryocytopoiesis.Flow cytometry(FCM) and laser cofocal technique were used to detect the expression of LAIR-1,the proliferation of cells was detected with CCK-8,the effect of LAIR-1 on the apoptosis of cells was analyzed by FCM with Annexin V-FITC/PI staining,and the impact of LAIR-1 on the cell ploidy was determined by FCM with PI staining.It was demonstrated that the expression of LAIR-1 on the cell membrane of Dami was rather low,but PMA could significantly induce its expression.In contrast to the control group,the cell proliferation of cells was decreased and cell apoptosis was increased after cross-linkage of LAIR-1 with specific antibody or ligand.During cell differentiation,the predominate cells were 2N and 4N,and the expression of CD41a and CD42b on these cells were reduced.It is evident that PMA can significantly induce the expression of LAIR-1 on the cell membrane of Dami.And the expression of LAIR-1 can inhibit the proliferation of the cell,stimulate its apoptosis,hinder the duplication of DNA and suppress the expression of CD41a and CD42b on the cells.
出处 《现代免疫学》 CAS CSCD 北大核心 2011年第4期285-290,共6页 Current Immunology
基金 国家自然科学基金资助项目(81001300) 山东省自然科学基金资助项目(Y2007C009) 山东省优秀中青年科学家科研奖励基金资助项目(2008BS03013)
关键词 LAIR-1 巨核细胞 Dami PMA LAIR-1 megakaryocytes Dami PMA
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参考文献16

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二级参考文献15

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共引文献11

同被引文献12

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