caa a22 4500 445376783 CHVBK 20180317143005.0 cr unu---uuuuu 170323e20110301xx s 000 0 eng 10.1007/s00702-010-0490-8 doi (NATIONALLICENCE)springer-10.1007/s00702-010-0490-8 Nuclear translocation of anamorsin during drug-induced dopaminergic neurodegeneration in culture and in rat brain [Elektronische Daten] [Kyung-Ah Park, Nuri Yun, Dong-Ik Shin, So Choi, Hyun Kim, Won-Ki Kim, Yuzuru Kanakura, Hirohiko Shibayama, Young Oh] Anamorsin, also called cytokine-induced apoptosis inhibitor 1 (CIAPIN1), was recently identified to confer resistance to apoptosis induced by growth factor deprivation and to be indispensible for hematopoiesis. Recently, it was demonstrated that anamorsin is also widely distributed in both fetal and adult tissues. In this study, we evaluated the tissue distribution of anamorsin in the central nervous system (CNS) during development. In situ hybridization and immunoblot analyses revealed that anamorsin mRNA and protein were both highly and widely expressed in various regions of the CNS, including the cerebral cortex, hippocampus, midbrain, cerebellum, medulla, and spinal cord. Based on these findings, we examined its cellular localization during drug-induced neurodegeneration in MN9D dopaminergic cells. Both immunocytochemical localization and immunoblot analyses indicated that cytosolic anamorsin was translocated into the nucleus in a time-dependent manner following treatment with a reactive oxygen species (ROS)-inducing drug, 6-hydroxydopamine (6-OHDA). Treatment of cells with the apoptosis-inducing reagent, staurosporine, did not appear to cause translocation of anamorsin into the nucleus. When cells were treated with the nuclear export inhibitor, Leptomycin B, alone or with 6-OHDA, nuclear anamorsin levels increased, indicating that nuclear influx and efflux of anamorsin are regulated by 6-OHDA treatment. In rat brain injected with 6-OHDA, nuclear translocation of anamorsin was identified in certain tyrosine hydroxylase (TH)-positive neurons as well as TH-negative cells. Furthermore, treatment of MN9D cells with hydrogen peroxide or ROS-inducing trace metals caused nuclear translocation of anamorsin. Taken together, our data indicate that nuclear translocation of anamorsin is a ROS-dependent event and may participate in the regulation of transcription of critical molecules during dopaminergic neurodegeneration. Springer-Verlag, 2010 Anamorsin nationallicence 6-Hydroxydopamine nationallicence Trace metal elements nationallicence Reactive oxygen species nationallicence Nuclear translocation nationallicence Neurodegeneration nationallicence Park Kyung-Ah Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut Yun Nuri Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut Shin Dong-Ik Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut Choi So Department of Anatomy and Brain Korea 21 Biomedical Science Program, Korea University College of Medicine, 136-705, Seoul, Korea aut Kim Hyun Department of Anatomy and Brain Korea 21 Biomedical Science Program, Korea University College of Medicine, 136-705, Seoul, Korea aut Kim Won-Ki Department of Anatomy and Brain Korea 21 Biomedical Science Program, Korea University College of Medicine, 136-705, Seoul, Korea aut Kanakura Yuzuru Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan aut Shibayama Hirohiko Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan aut Oh Young Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut Journal of Neural Transmission Springer Vienna 118/3(2011-03-01), 433-444 0300-9564 118:3<433 2011 118 702 https://doi.org/10.1007/s00702-010-0490-8 text/html Onlinezugriff via DOI 1 research-article jats NATIONALLICENCE 856 40 https://doi.org/10.1007/s00702-010-0490-8 text/html Onlinezugriff via DOI NATIONALLICENCE 700 1- Park Kyung-Ah Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut NATIONALLICENCE 700 1- Yun Nuri Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut NATIONALLICENCE 700 1- Shin Dong-Ik Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut NATIONALLICENCE 700 1- Choi So Department of Anatomy and Brain Korea 21 Biomedical Science Program, Korea University College of Medicine, 136-705, Seoul, Korea aut NATIONALLICENCE 700 1- Kim Hyun Department of Anatomy and Brain Korea 21 Biomedical Science Program, Korea University College of Medicine, 136-705, Seoul, Korea aut NATIONALLICENCE 700 1- Kim Won-Ki Department of Anatomy and Brain Korea 21 Biomedical Science Program, Korea University College of Medicine, 136-705, Seoul, Korea aut NATIONALLICENCE 700 1- Kanakura Yuzuru Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan aut NATIONALLICENCE 700 1- Shibayama Hirohiko Department of Hematology and Oncology, Osaka University Graduate School of Medicine, 565-0871, Osaka, Japan aut NATIONALLICENCE 700 1- Oh Young Department of Biology, Yonsei University College of Life Science and Biotechnology, 134 Shincheon-dong Seodaemoon-gu, 120-749, Seoul, Korea aut NATIONALLICENCE 773 0- Journal of Neural Transmission Springer Vienna 118/3(2011-03-01), 433-444 0300-9564 118:3<433 2011 118 702 Metadata rights reserved Springer special CC-BY-NC licence nationallicence BK010053 XK010053 XK010000 NATIONALLICENCE NATIONALLICENCE NL-springer