- 作者: Chia-Wen Chang; Wan-Hua Tsai; Woei-Jer Chuang; Yee-Shin Lin; Jmnn-Jong Wu; Ching-Chuan Liu; Pei-Jane Tsai; Ming-T. Lin
- 作者服務機構: 1 institute of Basic Medical Sciences, National Cheng Kung University Medical College, Tainan, Taiwan; ; 2 Biochemistry, National Cheng Kung University Medical College, Tainan, Taiwan; ; 3 Microbiology and Immunology, National Cheng Kung University Medical College, Tainan, Taiwan; ; 4 Medical Laboratory Science and Biotechnology, National Cheng Kung University Medical College, Tainan, Taiwan; ; 5 Department of Pediatrics, National Cheng Kung University Medical College, Tainan, Taiwan; ; 6 Institute of Medical Sciences, School of Medicine, Tzu Chi University, Hualien, 97004, Taiwan
- 中文摘要: --
- 英文摘要: After streptococcal pyrogenic exotoxin B (SPE B) induces apoptosis, its fate is unknown. Using confocal time-course microscopy at 37 蚓, we detected green fluorescence 20 min after adding FITC-SPE B. Orange fluorescence, an indication of co-localization of SPE B with lysosomes which were labeled with a red fluorescent probe, was maximal at 40 min and absent by 60 min. SPE B was co-precipitated with clathrin, which is consistent with endocytotic involvement. Western blotting assay also indicated that uptake of SPE B was maximal at 40 min and disappeared after 60 min. However, in the presence of chloroquine, a lysosome inhibitor, the uptake of SPE B was not detectable. The disappearance of TCA-precipitated FITC-SPE B was parallel to the appearance of TCA soluble FITC-SPE B; in the presence of chloroquine, however, no SPE B degradation occurred. Chloroquine increased the level of SPE B-induced apoptosis by inhibiting the degradation of SPE B. These results suggest that the internalization and degradation of SPE B in cells may be a host defense system that removes toxic substances by sacrificing the exposed cells.
- 中文關鍵字: --
- 英文關鍵字: A549 cell, apoptosis, clathrin, internalization, SPE B