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The role of mitochondria in nitric oxide-mediated thymocyte apoptosis
Authors:Migita Kiyoshi  Tanaka Fumiko  Abiru Seigo  Ida Hiroaki  Izumi Yasumori  Kawakami Atsushi  Eguchi Katsumi
Affiliation:

a Clinical Research Center, National Nagasaki Medical Center, Kubara 2-1001-1, Omura 856-8652, Japan

b First Department of Internal Medicine, Nagasaki University School of Medicine, Sakamoto 1-7-1, Nagasaki 852-8501, Japan

Abstract:The aim of this study was to analyze whether immunosuppressants could affect NO-induced thymocytes apoptosis. S-Nitroso-N-acetyl-D,L-penicillamine (SNAP, an NO donor) has an apoptotic effect on murine thymocytes. This NO-induced thymocyte apoptosis is associated with a reduced uptake of DiOC(6), a fluorochrome which incorporates into cells depending on their mitochondrial membrane potential (DeltaPsi(m)). The immunosuppressant, cyclosporin A, partially inhibited NO-induced thymocyte apoptosis as well as the reduction of DeltaPsi(m). In contrast, another immunosuppressant, FK506, did not affect NO-induced thymocyte apoptosis. Although FK506 and cyclosporin A inhibit T-cell signal transduction by the same mechanism, their effects on mitochondria may contribute to the differential apoptosis induction ability.
Keywords:Apoptosis   Cyclosporin A   FK506   Nitric oxide   Mitochondria
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