中国动脉硬化杂志2017，Vol.25Issue(5)：433-440,8.
LDLR缺失促进CD11b+ Ly6C+单核细胞的分化和CD11c+树突状细胞的成熟
LDLR deficiency promotes the differentiation of CD11b+Ly6C+ monocytes and maturation of CD11c+ dendritic cells
摘要
Abstract
Aim To identify the role of low density lipoprotein receptor (LDLR) on the proliferation and differentiation of CD11b9 myeloid subsets,particularly CD 1 1 b+ Gr-1 + immature myeloid cells with LDLR deficiency mice;To explore the mechanism of abnormal immune cell reaction in the pathogenesis of atherosclerosis.Methods 6-8 weeks old LDLR-/-mice and control wild type (WT) C57 mice were fed with normal diet and high-fat diet for 12 weeks.Flow cytometry was used to analyze the subsets of immune cells in peripheral blood,spleen and bone manow,especially the expressions of CD11b+ Gr-1+ myeloid immune cell,CD11b+ Ly6C+ mononuclear macrophage and CD11b+ CD11c+ dendritic cell.Simultaneously the expression of Lin-Sca-1-CD34+ cKit+ common myeloid progenitor (CMP) was detected in LDLR-/-mouse bone marrow.Using 125I marker anti-CD11b as a molecular probe,inflammatory microenvironment of LDLR-/-mice aortic atherosclerotic plaque was monitored noninvasively in vivo.Results (1) Under the condition of normal diet and high-fat diet,LDLR deficiency markedly enhanced the expressions CD 11b+ and CD11 b+ Gr-1 + myeloid cells in peripheral blood and spleen of LDLR-/-mice.(2)The expression of CD11 b+ Ly6C+ mononuclear macrophages increased in peripheral blood and liver of LDLR-/-mice;The expression of CD11b+CD11c+ dendritic cells increased in the spleen of LDLR-/-mice.(3) Under normal diet,the percentage of CMP was increased in LDLR-/-mice bone marrow compared with WT mice,but decreased under high-fat diet.(4) Using CD11 b as the molecular target of inflammation,SPECT/CT could be used to monitor the atherosclerotic plaque of LDLR-/-mouse in real time.Conclusion LDLR deficiency significantly increases the proliferation and mobilization of CD11 b+ Gr-1+ myeloid immune cells,and promotes the differentiation of mononuclear macrophage and maturation of dendritic cell in LDLR-/-mice.With CD11 b+ myeloid cells as a target,the inflammatory microenvironment of atherosclerotic plaques can be monitored in vivo.关键词
动脉粥样硬化/低密度脂蛋白受体/不成熟髓系细胞/共同髓系祖细胞/单核巨噬细胞/树突状细胞/炎症Key words
Atherosclerosis/Low density lipoprotein receptor/Immature myeloid cell/Common myeloid progenitor/Mononuclear macrophage/Dendritic cell/Inflammation分类
医药卫生引用本文复制引用
童明宏,张伟伟,王向明,张欢欢,陶荣霞,李盈,丁素玲,杨向东..LDLR缺失促进CD11b+ Ly6C+单核细胞的分化和CD11c+树突状细胞的成熟[J].中国动脉硬化杂志,2017,25(5):433-440,8.基金项目
国家自然科学基金项目(91439121、81370402) （91439121、81370402）
高等学校博士学科点专项科研基金资助课题(20130071110042) （20130071110042）
上海市长宁区科学技术委员会项目(CNKW2013J09) （CNKW2013J09）
