Mitochondria Play a Role in the Development of Non-Apoptotic Programmed Cell Death of Neutrophils Induced by ONO-AE-248  

作　　者：Jiajia Liu Hao He Zi Zhang Shixu Jiang Tohru Akahoshi Jian Yang Juan Li Tao He 

机构地区：[1]Laboratory of Molecular Biology, Luzhou Medical College, Luzhou, Sichuan 646000, China [2]Department of Immunology, Luzhou Medical College, Luzhou, Sichuan 646000, China [3]Department of Pathology of Kitasato University, 1-15-1 Kitasato, Sagamihara, Kanagawa, 228-8555 Japan [4]Department of Internal Medicine of Kitasato University of Japan, 1-15-1 Kitasato, Sagamihara, Kanagawa, 228-8555 Japan

出　　处：《Cellular & Molecular Immunology》2007年第6期447-453,共7页中国免疫学杂志（英文版）

基　　金：supported by grants from the National Natural Science Foundation of China(No.30371305).

摘　　要：We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. However, the mechanism of the neutrophil death is unclear. By using Western blotting, flow cytometry （FACS） and confocal laser scanning microscopy （CLSM）, we investigated the cellular signal transduction pathways of the neutrophil death. The research results showed that the neutrophil death induced by ONO-AE-248 did not show the morphologic changes of apoptosis and was not associated with the activity of caspase-3, caspase-8, and phosphorylation of p38-MAPK. However, impairment of mitochondria transmembrane potential has been found during the process of cell death. These findings suggested that ONO-AE-248 induced a non-apoptotic programmed cell death of neutrophils through partially mitochondria signaling transduction pathway. Cellular ＆ Molecular Immunology.We previously reported that ONO-AE-248, a selective EP3 receptor agonist, has been shown to cause neutrophil death without the typical features of apoptosis and necrosis. However, the mechanism of the neutrophil death is unclear. By using Western blotting, flow cytometry （FACS） and confocal laser scanning microscopy （CLSM）, we investigated the cellular signal transduction pathways of the neutrophil death. The research results showed that the neutrophil death induced by ONO-AE-248 did not show the morphologic changes of apoptosis and was not associated with the activity of caspase-3, caspase-8, and phosphorylation of p38-MAPK. However, impairment of mitochondria transmembrane potential has been found during the process of cell death. These findings suggested that ONO-AE-248 induced a non-apoptotic programmed cell death of neutrophils through partially mitochondria signaling transduction pathway. Cellular ＆ Molecular Immunology.

关 键 词：NEUTROPHIL ONO-AE-248 non-apoptotic programmed cell death mitochondria transmembrane potential 

分 类 号：R329.2[医药卫生—人体解剖和组织胚胎学]