| 引用本文： |
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刘少飞,匡雅姝,彭盛,等.单核细胞来源的微颗粒通过PPAR-α-SR-BI途径促进RAW264.7泡沫细胞形成的研究[J].同济大学学报（医学版）,2017,38(4):6-12. [点击复制]
- LIU Shao-fei,KUANG Ya-shu,PENG Sheng,et al.Monocyte-derived microparticles promote RAW264.7 foam cell formation via the PPAR-α-SR-BI pathway[J].同济大学学报（医学版）,2017,38(4):6-12. [点击复制]
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| 摘要: |
| 目的 研究单核细胞来源微颗粒对泡沫细胞形成的影响。方法 用氧化低密度脂蛋白或者低密度脂蛋白刺激RAW264.7细胞形成泡沫细胞,采用油红染色法对阳性的泡沫细胞进行染色,通过real-time PCR和Western印迹法测定微颗粒对RAW264.7细胞的受体或酶CD36、SR-A、ACAT1、nCEH、ABCA1、ABCG1、SR-BI的影响。结果 单核细胞来源的微颗粒影响RAW264.7细胞的活力；单核细胞来源的微颗粒可促进RAW264.7细胞的泡沫化形成；低浓度(20μl/ml)微颗粒可轻微促进巨噬细胞对低密度脂蛋白的吞噬,但对氧化低密度脂蛋白的吞噬却没有影响；过氧化物酶体增殖物激活受体-α(PPAR-α)的激动剂可增强泡沫细胞形成,拮抗剂作用相反。单核细胞来源微颗粒可下调SR-BI在mRNA和蛋白质水平的表达。PPAR-α激动剂可下调单核细胞来源微颗粒对RAW264.7巨噬细胞中SR-BI蛋白表达,PPAR-α拮抗剂没有影响。结论 单核细胞来源的微颗粒通过引起过氧化物酶体增殖物激活受体-α的表达,进而使巨噬细胞表面SR-BI的表达降低,从而促进RAW264.7泡沫细胞形成。 |
| 关键词: 单核细胞微颗粒 巨噬细胞 泡沫细胞 过氧化物酶体增殖物激活受体-α 动脉粥样硬化 |
| DOI：10.16118/j.1008-0392.2017.04.002 |
| 投稿时间：2016-12-29 |
| 基金项目:上海市浦东新区科委课题(PKJ2013-Y19) |
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| Monocyte-derived microparticles promote RAW264.7 foam cell formation via the PPAR-α-SR-BI pathway |
| LIU Shao-fei,KUANG Ya-shu,PENG Sheng,YAN Jian-she,LI Ying |
| (Dept.of Cardiology, East Hospital, Tongji University, School of Medicine, Shanghai 200120, China;Shanghai Institute of Immunology, Shanghai Jiaotong University, Shanghai 200025, China) |
| Abstract: |
| Objective To investigate the role of the monocyte-derived microparticles (mono-MPs) in the formation of foam cells. Methods Mouse macrophage RAW264.7 cells were stimulated with oxidized low density lipoprotein or low density lipoprotein to form foam cells. Positive foam cells were stained with oil red staining. Real-time PCR and Western blotting were used to determine RAW264.7 Cell receptor or enzyme CD36, SR-A, ACAT1, nCEH, ABCA1, ABCG1, SR-BI. Results Mono-MPs affected the activity of RAW264.7 cells. Mono-MPs promoted the formation of RAW264.7 foam cells; low concentration (20μl/ml) microparticles slightly promoted the phagocytosis of macrophages to low-density lipoproteins, but did not affect the intake of oxidized low-density lipoproteins. Peroxisome proliferator-activated receptor-alpha (PPAR-α) agonists enhanced foam cells formation, while the effect of PPAR-α antagonist was reversed. Mono-MPs reduced the expression of SR-BI mRNA and protein levels. PPAR-α agonists reduced the expression of SR-BI protein in RAW264.7 macrophages, while PPAR-α antagonist had no effect. Conclusion The mono-MPs, causing activation of the PPAR-α, induce the RAW264.7 foam cell formation via lipid uptake and the PPAR-α-SR-BI pathway. |
| Key words: monocyte-derived microparticles macrophage foam cell PPAR-α atherosclerosis |
