WEN Liang, LI Jie, ZHANG Min-xia, XUE Qiang. Macrophage migration inhibitory factor mediated effect of oxidized low density lipoprotein on endothelial cell function and its mechanism[J]. Chinese Heart Journal, 2023, 35(6): 629-636. DOI: 10.12125/j.chj.202208094
    Citation: WEN Liang, LI Jie, ZHANG Min-xia, XUE Qiang. Macrophage migration inhibitory factor mediated effect of oxidized low density lipoprotein on endothelial cell function and its mechanism[J]. Chinese Heart Journal, 2023, 35(6): 629-636. DOI: 10.12125/j.chj.202208094

    Macrophage migration inhibitory factor mediated effect of oxidized low density lipoprotein on endothelial cell function and its mechanism

    • AIM To investigate macrophage migration inhibitory factor (MIF) mediated effect of oxidized low density lipoprotein (ox-LDL) on vascular endothelial cell function and its mechanism.
      METHODS Human umbilical vein endothelial cells (HUVECS) were treated with ox-LDL (100 nmol/L) and the expression and function of related proteins were detected by immunoelectrophoresis. Real-time quantitative PCR was used to monitor the expression of inflammatory factors and the effects of drug blockade and gene intervention on the expression of downstream genes were observed. Griess response was used to monitor NO production in endothelial cells under the intervention. Ex vivo, acetylcholine-induced vasodilation was used as an indicator of endothelium-dependent vasodilation to detect endothelial cell function.
      RESULTS ox-LDL increased the expression of sterol regulatory element binding protein (SREBP2) and MIF, and either drug specific blockage or siRNA inhibition of MIF expression significantly reduced the expression and activation of SREBP2 (P<0.05). MIF regulated vascular endothelial cell function through SREBP2 (P<0.05).
      CONSCLUSIONS  Oxidative stress such as ox-LDL can increase the expression of SREBP2-mediated inflammasome and inflamma-related adhesion molecules on endothelial cells through MIF, thereby disrupting endothelial cell function, which is one of the important mechanisms for the occurrence and development of atherosclerosis.
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