Oxidized low-density lipoprotein alters endothelial progenitor cell populations

Authors

    Authors

    Y. Q. Cui; C. A. Narasimhulu; L. J. Liu; X. Li; Y. Xiao; J. Zhang; X. Y. Xie; H. Hao; J. Z. Liu; G. L. He; P. J. Cowan; L. Q. Cui; H. Zhu; S. Parthasarathy;Z. G. Liu

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    Abbreviated Journal Title

    Front. Biosci.

    Keywords

    ox-LDL; hyperlipidemia; NAC; ROS; EPC; CORONARY-ARTERY DISEASE; SMOOTH-MUSCLE-CELLS; MARROW STEM-CELLS; NEOINTIMA FORMATION; PERIPHERAL-BLOOD; VASCULAR BIOLOGY; OXIDATIVE; STRESS; PROTEIN-KINASE; HEART-FAILURE; PLASMA-LEVELS; Biochemistry & Molecular Biology; Cell Biology

    Abstract

    Oxidized low-density lipoprotein (ox-LDL) is critical to atherosclerosis in hyperlipidemia. Bone marrow (BM)-derived endothelial progenitor cells (EPCs) are important in preventing atherosclerosis, however these cells are significantly decreased in number in hyperlipidemia. This study aimed to determine whether ox-LDL and hyperlipidemia exert similar effects on EPC populations, and to investigate the involvement of reactive oxygen species (ROS). ROS production in BM and blood was significantly increased in male C57BL/6 mice treated with intravenous ox-LDL, and in hyperlipidemic LDL receptor knockout mice fed with a 4-month high-fat diet. ROS formation was effectively blocked by overexpression of antioxidant enzymes or N-acetylcysteine treatment. In both hyperlipidemic and ox-LDL-treated mice, the number of c-Kit(+)/CD31(+) cells in BM and blood and of Sca-1(+)/Flk-1(+) cells in blood significantly decreased, whereas the number of blood Flk-1(+) cells increased. In contrast, the number of blood CD34(+)/CD133(+) cells increased in ox-LDL-treated mice but decreased in hyperlipidemic mice. Only the changes in CD34(+)/Flk-1(+) cell number were prevented by inhibiting ROS production. These data suggested that ox-LDL produced significant changes in BM and blood EPC populations, largely similar to chronic hyperlipidemia, via predominantly ROS-independent mechanism(s).

    Journal Title

    Frontiers in Bioscience-Landmark

    Volume

    20

    Publication Date

    1-1-2015

    Document Type

    Article

    Language

    English

    First Page

    975

    Last Page

    988

    WOS Identifier

    WOS:000354355900007

    ISSN

    1093-9946

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