WANG Yongfang
Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, ChinaPENG Zhuoying
Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, ChinaLI Xiang
Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, ChinaCONG Zhe
Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, ChinaXUE Jing
Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, ChinaWEI Qiang
Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, China(Comparative Medicine Center, Peking Union Medical College (PUMC) & Institute of Laboratory Animal Science (ILAS), Chinese Academy of Medical Sciences (CAMS); Key Laboratory of Human Diseases Comparative Medicine, Ministry of Health; Key Laboratory of Human Diseases Animal Models, State administration of Traditional Chinese Medicine; Beijing Key Laboratory for Animal Models of Emerging and Remerging Infectious Diseases, Beijing 100021, China)
R-33
Objective To investigate the effects of galectin?2, galectin?4, galectin?7, galectin?8, and galectin?9on the apoptosis in HIV?1?infected macrophages and to provide the theoretical and application basis for elimination of HIV?1?infected cellular reservoirs. Methods Firstly, apoptosis of human monocytic cell line THP?1 cells was induced bydifferent concentrations of galectins to determine the suitable concentration of different galetcins. Secondly, monocytes (THP?1) were stimulated to differentiate into macrophages (THP?1?Mφ) with phorbol myristate acetate (PMA), and then macrophages were prepared and infected with HIV?1. Finally, HIV?1?infected and uninfected macrophages were respectively treated with the suitable concentrations of galectin?2, galectin?4, galectin?7, galectin?8, galectin?9 and then the apoptosis in these macrophages was detected. Results The cell death rate of macrophages without treatment was 4.39 ±0.74%. The cell death rates of macrophages induced by 5 μmol/ L galectin?2, 5 μmol/ L galectin?4, 7.5 μmol/ L galectin?7, 3 μmol/ L galectin?8 and 1 μmol/ L galectin?9 were 4.78 ±0.41%, 7.21 ±1.46%, 3.78 ± 1.03%, 5.88 ±2.08%, 8.10 ±4.13%, respectively, with no statistically significant defferences among the groups ( P > 0.05). The cell death rate of HIV?1?infected macrophages without treatment was 12.69 ±1.16%, and that of HIV?1?infected macrophages induced by 5 μmol/ L galectin?2, 5 μmol/ L galectin?4, 7.5 μmol/ L galectin?7, 3 μmol/ L galectin?8 and 1 μmol/ L galectin?9 were 11.69 ±0.90%, 17.45 ±1.30%, 32.01 ±1.30%, 15.77 ±1.21% and 19.27 ±2.13%, respectively. There were significant differences between the control group and galectin?7?treated group ( P < 0.001). Conclusions Galectin?7?induces extensive apoptosis in HIV?1?infected macrophages but not in uninfected macrophages.
