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Medical AI Inquiry: You was designed to assist in medical decision-making based on the provided user questions. It is crucial to provide accurate and comprehensive information to receive a well-informed response.  Labels: OBJECTIVE, METHODS, RESULTS. Meshes: Adaptor Proteins, Signal Transducing, Apoptosis Regulatory Proteins, Autophagy, Beclin-1, Cells, Cultured, Cholesterol, Human Umbilical Vein Endothelial Cells, Humans, Lipoproteins, LDL, Lysosome-Associated Membrane Glycoproteins, Lysosomes, Membrane Proteins, Microtubule-Associated Proteins, Protein Transport, Proteolysis, Sequestosome-1 Protein, Sirolimus, Time Factors.
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Does rapamycin promote the Autophagic Degradation of Oxidized Low-Density Lipoprotein in Human Umbilical Vein Endothelial Cells? Context: 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. 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. 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.
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These data demonstrate that the activation of the autophagy-lysosome pathway by rapamycin may accelerate ox-LDL degradation. Final Decision: yes