| 脂肪酸结合蛋白4对BCG诱导巨噬细胞自噬的调控作用 |
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| 引用本文： | 于嘉霖,徐雅楠,韩璐,马沁梅,吴晓玲,邓光存.脂肪酸结合蛋白4对BCG诱导巨噬细胞自噬的调控作用[J].畜牧兽医学报,2020,51(9):2265-2274. |
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| 作者姓名： | 于嘉霖 徐雅楠 韩璐 马沁梅 吴晓玲 邓光存 |
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| 作者单位： | 1. 西部特色资源保护与利用教育部重点实验室, 银川 750021;2. 宁夏大学生命科学学院, 银川 750021 |
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| 基金项目： | 国家自然科学基金（31760326）；宁夏重点研发计划项目（2018BFH03017）；西部一流学科建设重大创新项目（ZKZD2017001）；宁夏科技创新领军人才培养项目（KJT2017002）；宁夏大学研究生创新项目（GIP2019067） |
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| 摘 要： | 旨在探讨脂肪酸结合蛋白4（fatty acid binding protein，FABP4）在牛分枝杆菌卡介苗（BCG）感染的巨噬细胞中对脂肪酸代谢与自噬的调控作用。本研究利用小干扰RNA技术敲减小鼠巨噬细胞系RAW264.7中FABP4的表达，并结合BCG感染，采用免疫印记和免疫荧光等技术，检测了FABP4蛋白表达、脂肪酸累积、脂肪酸β氧化和自噬相关蛋白表达等指标。结果表明，BCG感染极显著上调了小鼠巨噬细胞RAW264.7中FABP4的表达（P<0.001）并促进了脂肪酸的累积。FABP4小干扰RNA（siRNA-FABP4）能显著降低BCG感染后巨噬细胞中脂肪酸含量，伴随着肉毒碱棕榈酰移位酶1A（CPT1A）的表达上调（P<0.05），与ATP产量的提升（P<0.05）。同时，siRNA-FABP4极显著下调了自噬调控关键因子AMPK及自噬相关蛋白p-ULK1、ATG5、ATG7、ATG12和LC3B的表达（P<0.01）。以上研究结果表明，在BCG感染RAW264.7细胞过程中，下调了FABP4的表达，促进了脂肪酸的氧化，减少了巨噬细胞内脂肪酸的含量，并通过AMPK信号通路抑制了细胞自噬的发生。
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| 关 键 词： | FABP4 BCG 巨噬细胞RAW264.7 脂肪酸代谢 细胞自噬 |
| 收稿时间： | 2020-04-13 |
Role of Fatty Acid Binding Protein 4 in Regulating Macrophage Autophagy Induced by BCG Infection |
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| YU Jialin,XU Yanan,HAN Lu,MA Qinmei,WU Xiaoling,DENG Guangcun.Role of Fatty Acid Binding Protein 4 in Regulating Macrophage Autophagy Induced by BCG Infection[J].Acta Veterinaria et Zootechnica Sinica,2020,51(9):2265-2274. |
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| Authors: | YU Jialin XU Yanan HAN Lu MA Qinmei WU Xiaoling DENG Guangcun |
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| Institution: | 1. Key Lab of Ministry of Education for Protection and Utilization of Special Biological Rsources in Wstern China, Ningxia University, Yinchuan 750021, China;2. College of Life Science, Ningxia University, Yinchuan 750021, China |
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| Abstract: | To investigate the role of FABP4 on regulating fatty acid metabolism and autophagy in macrophage infected with BCG, small interfering RNA for FABP4 were transfected into RAW264.7 cells alone or combined with BCG infection. The immunoblot and immunofluorescence were used to detect the expression of FABP4, the accumulation of lipid droplets, the expression of fatty acid β-oxidation and autophagy related factors. The results showed that the infection of BCG increased the expression of FABP4 and accompanied with the accumulation of lipid droplets in RAW264.7. Moreover, the knockdown of FABP4 decreased lipid droplets but promoted the expression of carnitine palmitoyltransferase 1A (CPT1A) (P <0.05) and the production of ATP (P <0.05). Meanwhile, the knockdown of FABP4 suppressed the expression of AMPK, p-ULK1, ATG5, ATG7, ATG12 and LC3B which are autophagy related factors (P<0.001). Our results indicated that the knockdown of FABP4 promoted fatty acid oxidation, decreased fatty acid level and suppressed autophagy via AMPK signal pathway in BCG infected RAW264.7 cells. |
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| Keywords: | FABP4 BCG macrophage RAW264 7 fatty acid metabolism autophagy |
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