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  • Title: Rapamycin Promotes the Autophagic Degradation of Oxidized Low-Density Lipoprotein in Human Umbilical Vein Endothelial Cells.
    Author: Zhang Y, Han Q, You S, Cao Y, Zhang X, Liu H, Hu L, Liu CF.
    Journal: J Vasc Res; 2015; 52(3):210-9. PubMed ID: 26623657.
    Abstract:
    BACKGROUND/AIMS: Oxidized low-density lipoprotein (ox-LDL) has been extensively implicated in the initiation of atherosclerosis. Our previous studies reported that ox-LDL could activate autophagy in human umbilical vein endothelial cells (HUVECs). Because of this, subsequent studies were designed to elucidate the possible role of the autophagic inducer, rapamycin, on ox-LDL degradation in endothelial cells. METHODS: Intracellular cholesterol content was measured using a tissue total cholesterol assay kit. ox-LDL trafficking within endothelial cells was analyzed by flow cytometry. Levels of proteins involved in the autophagic process, microtubule-associated protein 1 light chain 3 (MAP1-LC3), lysosome-associated membrane protein 1 (LAMP1), Beclin 1 and p62, were assessed by Western blot analysis. RESULTS: We discovered that rapamycin could decrease the ox-LDL content in HUVECs at the 3-hour time point. Rapamycin also mediated an obvious increase in Dil-labeled ox-LDL (Dil-ox-LDL)/LC3 and Dil-ox-LDL/LAMP1 co-localization, which was inhibited by 3-methyladenine (3-MA), an autophagic inhibitor. In addition, significant co-localization of LC3 and LAMP1 occurred in cells pretreated with rapamycin. In the presence of rapamycin, p62 levels were reduced, and autophagic flux was enhanced. CONCLUSION: These data demonstrate that the activation of the autophagy-lysosome pathway by rapamycin may accelerate ox-LDL degradation.
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