Abstract
Sympathetic neurons undergo apoptosis when deprived of nerve growth factor (NGF). Inhibitors of RNA or protein synthesis block this death, suggesting that gene expression is important for apoptosis in this system. We have identified SM-20 as a new gene that increases in expression in sympathetic neurons after NGF withdrawal. Expression of SM-20 also increases during neuronal death caused by cytosine arabinoside or the phosphatidylinositol 3-kinase inhibitor LY294002. In addition, SM-20 protein synthesis is elevated in NGF-deprived neurons compared with neurons maintained with NGF. Importantly, expression of SM-20 in sympathetic neurons causes cell death in the presence of NGF. These results suggest that SM-20 may function to regulate cell death in neurons.
Publication types
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Research Support, Non-U.S. Gov't
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Animals
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Apoptosis* / drug effects
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Cells, Cultured
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Chromones / pharmacology
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Cytarabine / pharmacology
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DNA-Binding Proteins*
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Embryo, Mammalian
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Enzyme Inhibitors / pharmacology
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Gene Expression*
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Hypoxia-Inducible Factor-Proline Dioxygenases
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Immediate-Early Proteins / genetics*
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Immediate-Early Proteins / physiology
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Morpholines / pharmacology
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Nerve Growth Factors / administration & dosage
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Nerve Growth Factors / pharmacology*
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Neurons / chemistry
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Neurons / cytology
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Neurons / physiology*
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Phosphoinositide-3 Kinase Inhibitors
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RNA, Messenger / analysis
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Rats
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Reverse Transcriptase Polymerase Chain Reaction
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Superior Cervical Ganglion / cytology
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Transfection
Substances
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Chromones
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DNA-Binding Proteins
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Enzyme Inhibitors
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Immediate-Early Proteins
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Morpholines
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Nerve Growth Factors
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Phosphoinositide-3 Kinase Inhibitors
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RNA, Messenger
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Cytarabine
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2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
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Egln3 protein, rat
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Hypoxia-Inducible Factor-Proline Dioxygenases