國家衛生研究院 NHRI:Item 3990099045/12376
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    題名: Vanadium derivative exposure promotes functional alterations of VSMCs and consequent atherosclerosis via ROS/p38/NF-kappaB-Mediated IL-6 Production
    其他題名: Vanadium derivative exposure promotes functional alterations of VSMCs and consequent atherosclerosis via ROS/p38/NF-κB-Mediated IL-6 Production
    作者: Yeh, CC;Wu, JY;Lee, GL;Wen, HT;Lin, P;Kuo, CC
    貢獻者: Institute of Cellular and Systems Medicine;National Institute of Environmental Health Sciences
    摘要: Vanadium is a transition metal widely distributed in the Earth's crust, and is a major contaminant in fossil fuels. Its pathological effect and regulation in atherosclerosis remain unclear. We found that intranasal administration of the vanadium derivative NaVO3 significantly increased plasma and urinary vanadium levels and induced arterial lipid accumulation and atherosclerotic lesions in apolipoprotein E-deficient knockout mice (ApoE-/-) murine aorta compared to those in vehicle-exposed mice. This was accompanied by an increase in plasma reactive oxygen species (ROS) and interleukin 6 (IL-6) levels and a decrease in the vascular smooth muscle cell (VSMC) differentiation marker protein SM22α in the atherosclerotic lesions. Furthermore, exposure to NaVO3 or VOSO4 induced cytosolic ROS generation and IL-6 production in VSMCs and promoted VSMC synthetic differentiation, migration, and proliferation. The anti-oxidant N-acetylcysteine (NAC) not only suppresses IL-6 production and VSMC pathological responses including migration and proliferation but also prevents atherosclerosis in ApoE-/- mice. Inhibition experiments with NAC and pharmacological inhibitors demonstrated that NaVO3-induced IL-6 production is signaled by ROS-triggered p38-mediated NF-κB-dependent pathways. Neutralizing anti-IL-6 antibodies impaired NaVO3-mediated VSMC migration and proliferation. We concluded that NaVO3 exposure activates the ROS-triggering p38 signaling to selectively induce NF-κB-mediated IL-6 production. These signaling pathways induce VSMC synthetic differentiation, migration, and proliferation, leading to lipid accumulation and atherosclerosis.
    日期: 2019-12
    關聯: International Journal of Molecular Sciences. 2019 Dec 20(24):Article number 6115.
    Link to: http://dx.doi.org/10.3390/ijms20246115
    JIF/Ranking 2023: http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=1422-0067&DestApp=IC2JCR
    Cited Times(WOS): https://www.webofscience.com/wos/woscc/full-record/WOS:000506840100010
    Cited Times(Scopus): https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85076302816
    顯示於類別:[郭呈欽] 期刊論文
    [林嬪嬪] 期刊論文

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