Effects of HDL from patients with coronary artery disease on lipid deposition and apoptosis in mouse peritoneal macrophages |
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| Authors: | WANG Yuan GAO Hong-wei FENG Gao-jie DAI Pei ZHANG Qin-feng BAI Rui QIN Wei-wei LI Hong GAO Fen |
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| Institution: | The Second Clinical College of Shanxi Medical University, Taiyuan 030001, China |
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| Abstract: | AIM: To compare the effects of high-density lipoprotein (HDL) from healthy subjects (HDLheathy) and HDL from the patients with coronary artery disease (HDLCAD) on the lipid deposition and apoptosis in mouse peritoneal macrophages. METHODS: HDL was isolated from healthy subjects, stable CAD patients (HDLSCAD) and acute myocar-dial infarction patients (HDLAMI). The accumulation of intracellular lipids was determined by oil red O staining. The apoptosis of macrophages was measured by fluorescence microscopy with annexin-V/PI staining. DCHF-DA, a redox-sensitive dye, was used to detect intracellular reactive oxygen species (ROS) levels. The protein expression of ATP-binding cassette transporter (ABC) A1, ABCG1, Bcl-2 and Bax was determined by Western blot analysis. RESULTS: Lipid deposition in the macrophages was increased significantly after oxidized low-density lipoprotein (ox-LDL) treatment, and the expression of ABCA1 and ABCG1 was up-regulated (P<0.05). Compared with ox-LDL treatment alone, HDLhealthy decreased lipid deposition in the macrophages and up-regulated the expression of ABCA1 and ABCG1 (P<0.05), while treatment with HDLSCAD or HDLAMI further decreased lipid deposition in the macrophages and down-regulated the expression of ABCA1 and ABCG1 (P<0.05). Compared with HDLSCAD treatment, lipid deposition in the macrophages was further increased after HDLAMI treatment, and the expression of ABCA1 and ABCG1 was down-regulated (P<0.05). HDLhealthy decreased the levels of intracellular ROS and apoptosis by increasing the level of antiapoptotic protein Bcl-2 and reducing the expression of proapoptotic protein Bax. In contrast, HDLSCAD and HDLAMI had opposite effects on the intracellular ROS, the cell apoptosis and the expression of apoptosis-related proteins Bcl-2 and Bax. CONCLUSION: HDLCAD promotes lipid accumulation in macrophages and induces macrophage apoptosis. These findings provide novel insights into mechanisms leading to altered vascular effects of HDL in CAD. |
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| Keywords: | Coronary artery disease High-density lipoprotein ATP-binding cassette transporters Apoptosis |
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