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    The persistence of low-grade inflammatory monocytes contributes to aggravated Atherosclerosis

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    Date
    2016-11-08
    Author
    Geng, Shuo
    Chen, Keqiang
    Yuan, Ruoxi
    Maitra, Urmila
    Na, Diao
    Chen, Chun
    Zhang, Yao
    Li, Liwu
    et al.
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    Abstract
    Sustained low-grade inflammation mediated by non-resolving inflammatory monocytes has long been suspected in the pathogenesis of atherosclerosis; however, the molecular mechanisms responsible for the sustainment of non-resolving inflammatory monocytes during atherosclerosis are poorly understood. Here we observe that subclinical endotoxemia, often seen in humans with chronic inflammation, aggravates murine atherosclerosis through programming monocytes into a non-resolving inflammatory state with elevated Ly6C, CCR5, MCP-1 and reduced SR-B1. The sustainment of inflammatory monocytes is due to the disruption of homeostatic tolerance through the elevation of miR-24 and reduction of the key negative-feedback regulator IRAK-M. miR-24 reduces the levels of Smad4 required for the expression of IRAK-M and also downregulates key lipid-processing molecule SR-B1. IRAK-M deficiency in turn leads to elevated miR-24 levels, sustains disruption of monocyte homeostasis and aggravates atherosclerosis. Our data define an integrated feedback circuit in monocytes and its disruption may lead to non-resolving low-grade inflammation conducive to atherosclerosis.
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    http://hdl.handle.net/10919/80354
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    • Research Articles, Department of Biological Sciences [305]

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