| Motor neuron degeneration is attenuated in bax-deficient neurons in vitro. | |
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MedLine Citation:
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PMID: 10082077 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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Apoptosis plays a major role in motor neuron survival during developmental cell death, after axotomy, and in motor neuron diseases. Bax is the first member of the bcl-2 family shown to promote apoptosis. In the present study, we used the bax-deficient mouse model to determine the role of bax in motor neuron survival in vitro by using dissociated spinal cord cultures. This system enables the maturation of individual motor neurons in a controlled in vitro environment. Motor neurons were identified by using the antineurofilament antibody SMI-32 and the antitranscription factor antibody Islet1. Both antibodies labeled large motor neurons in wild-type and bax-null cultures. Differentiated wild-type cultures exhibited a reduction in long-term cultures of two- and fivefold in the number of SMI-32- and Islet1-positive cells, respectively. The reduction in the number of motor neurons was attenuated in bax -/- cultures. Bax deficiency also attenuated serum withdrawal- and kainate-induced apoptosis in motor neurons. For comparison, necrotic cell death led to significant motor neuron cell death in both wild-type and bax -/- cultures. In addition, bax deficiency did not induce proliferation of motor neuron precursors in vitro. This study indicates for the first time that bax has a dominant role in the survival of long-term cultured motor neurons. |
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Authors:
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O Bar-Peled; M Knudson; S J Korsmeyer; J D Rothstein |
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Publication Detail:
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Type: Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S. |
Journal Detail:
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Title: Journal of neuroscience research Volume: 55 ISSN: 0360-4012 ISO Abbreviation: J. Neurosci. Res. Publication Date: 1999 Mar |
Date Detail:
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Created Date: 1999-05-24 Completed Date: 1999-05-24 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 7600111 Medline TA: J Neurosci Res Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 542-56 Citation Subset: IM |
Affiliation:
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Department of Neurology, Johns Hopkins University, Baltimore, Maryland 21287-7519, USA. |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Aspartic Acid / analogs & derivatives, pharmacology Astrocytes / cytology, metabolism Cell Death / drug effects Cell Division / drug effects Cell Nucleus / drug effects, metabolism Cell Size Cell Survival / drug effects Cells, Cultured Culture Media, Serum-Free Female Genotype Kainic Acid / antagonists & inhibitors, pharmacology Male Mice Motor Neurons / cytology, drug effects, metabolism, pathology* Nerve Degeneration* Paraquat / pharmacology Proto-Oncogene Proteins / deficiency, genetics, physiology* Proto-Oncogene Proteins c-bcl-2* Spinal Cord / cytology, embryology Superoxides / metabolism bcl-2-Associated X Protein |
| Grant Support | |
ID/Acronym/Agency:
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AG12992/AG/NIA NIH HHS; NS33958/NS/NINDS NIH HHS; NS34100/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/Bax protein, mouse; 0/Culture Media, Serum-Free; 0/Proto-Oncogene Proteins; 0/Proto-Oncogene Proteins c-bcl-2; 0/bcl-2-Associated X Protein; 11062-77-4/Superoxides; 1860-87-3/3-hydroxyaspartic acid; 4685-14-7/Paraquat; 487-79-6/Kainic Acid; 56-84-8/Aspartic Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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