A rapid loss of mitochondrial membrane potential stimulated by ONO--AE--248 induces non--apoptotic programmed cell death of neutrophils
Zhang Zi, Jiajia Liu, He Hao, Yijun Huang, Juan Li, Xie Huafu, Tao He, Zhao Jing
Abstract
Zhang Zi, Jiajia Liu, He Hao, Yijun Huang, Juan Li, Xie Huafu, Tao He, Zhao Jing
Abstract
Objective To investigate the changes and roles of mitochondria in neutrophil death induced by ONO-AE-248. Me- thods Human neutrophils were cultured in vitro with ONO-AE-248(5×10~ -5 mol/L)and medium, respectively. FACS and confocal microscopy were used to detect the mitochondria structure and flow cytometry was employed to detect the level of mitochondria membrane potential. Re- sults ONO -AE-248 resulted in a rapid loss of mitochondrial membrane potential of neutrophils. The mitochondrial structure and distribution also were obviously different between spontaneous apoptosis and non-apoptosis programmed cell death induced by ONO-AE-248. Conclu- sion The experiment results suggest that changes of mitochondrial structure and function might be a typical morphological, physiological, and biochemical feature in this unique form of neutrophil death, and that the mitochondrial pathway might play an important role in ONO-AE-248-induced death of neutrophils.
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Objective To investigate the changes and roles of mitochondria in neutrophil death induced by ONO-AE-248. Me- thods Human neutrophils were cultured in vitro with ONO-AE-248(5×10~ -5 mol/L)and medium, respectively. FACS and confocal microscopy were used to detect the mitochondria structure and flow cytometry was employed to detect the level of mitochondria membrane potential. Re- sults ONO -AE-248 resulted in a rapid loss of mitochondrial membrane potential of neutrophils. The mitochondrial structure and distribution also were obviously different between spontaneous apoptosis and non-apoptosis programmed cell death induced by ONO-AE-248. Conclu- sion The experiment results suggest that changes of mitochondrial structure and function might be a typical morphological, physiological, and biochemical feature in this unique form of neutrophil death, and that the mitochondrial pathway might play an important role in ONO-AE-248-induced death of neutrophils.
Key concepts: Apoptosis, Mitochondrion, Programmed cell death, Cell biology, Flow cytometry, Membrane potential, Biology, Cell