Abstract
Recent evidence from apolipoprotein E-deficient (apoE−/−) mice shows that aging and atherosclerosis are closely associated with increased oxidative stress and DNA damage in some cells and tissues. However, bone marrow cells, which are physiologically involved in tissue repair have not yet been investigated. In the present study, we evaluated the influence of aging and hypercholesterolemia on oxidative stress, DNA damage and apoptosis in bone marrow cells from young and aged apoE−/− mice compared with age-matched wild-type C57BL/6 (C57) mice, using the comet assay and flow cytometry. The production of both superoxide and hydrogen peroxide in bone marrow cells was higher in young apoE−/− mice than in age-matched C57 mice, and reactive oxygen species were increased in aged C57 and apoE−/− mice. Similar results were observed when we analyzed the DNA damage and apoptosis. Our data showed that both aging and hypercholesterolemia induce the increased production of oxidative stress and consequently DNA damage and apoptosis in bone marrow cells. This study is the first to demonstrate a functionality decrease of the bone marrow, which is a fundamental extra-arterial source of the cells involved in vascular injury repair.
Highlights
Atherosclerosis is a progressive disease that results from lipid disorders, enhanced oxidative stress and inflammation [1,2]
Several studies [2,12,13,15,24] have shown that chronic injuries to the arterial wall in apoE−/− mice contribute to the development of atherosclerosis
The results obtained in the present study might clarify how hypercholesterolemia and aging might compromise the viability of the bone marrow to produce the vascular progenitor cells responsible for arterial repair
Summary
Atherosclerosis is a progressive disease that results from lipid disorders, enhanced oxidative stress and inflammation [1,2]. DNA is another cellular target of ROS, resulting in detrimental effects, including the activation of inflammation, cell apoptosis and aging in diverse tissues and organs [9,10]. Oxidative stress and DNA damage in bone marrow mononuclear cells (MNC), which are physiologically involved in tissue repair [18]. To evaluate the effects of aging and hypercholesterolemia on oxidative stress, DNA damage and apoptosis. Despite these advances, the effects of these events in bone marrow MNC have not yet been investigated in the murine model of spontaneous hypercholesterolemia and atherosclerosis. The aim of this study was to examine the hypothesis that aging and hypercholesterolemia are associated with the enhanced production of ROS, DNA damage and apoptosis in bone marrow.
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