| Growth hormone prevents apoptosis through activation of nuclear factor-kappaB in interleukin-3-dependent Ba/F3 cell line. | |
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MedLine Citation:
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PMID: 10809229 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The pro-B Ba/F3 cell line requires interleukin-3 and serum for growth, and their removal results in cell apoptosis. Ba/F3 cells transfected with the GH receptor (GHR) cDNA become able to proliferate in response to GH. To investigate the role of GH in the control of apoptosis, Ba/F3 cells expressing either the wild-type rat GHR (Ba/F3 GHR) or a mutated rat GHR (Ba/F3 ILV/T) were used. We show that Ba/F3 GHR cells, but not parental Ba/F3 or Ba/F3 ILV/T cells, were able to survive in the absence of growth factor. Furthermore, an autocrine/paracrine mode of GH action was suggested by the demonstration that Ba/F3 cells produce GH, and that addition of GH antagonists (B2036 and G120K) promotes apoptosis of Ba/F3 GHR cells. Consistent with survival, the levels of both antiapoptotic proteins Bcl-2 and Bag-1 were maintained in Ba/F3 GHR cells, but not in parental Ba/F3 cells upon growth factor deprivation. Constitutive activation of the transcription factor nuclear factor-kappaB (NF-kappaB), which has been shown to promote cell survival, was sustained in Ba/F3 GHR cells, whereas no NF-kappaB activation was detected in parental Ba/F3 cells in the absence of growth factor. Furthermore, addition of GH induced NF-kappaB DNA binding activity in Ba/F3 GHR cells. Overexpression of the mutated IkappaB alpha (A32/36) protein, known to inhibit NF-kappaB activity, resulted in death of growth factor-deprived Ba/F3 GHR cells, and addition of GH was no longer able to rescue these cells from apoptosis. Together, our results provide evidence for a new GH-mediated pathway that initiates a survival signal through activation of the transcription factor NF-kappaB and sustained levels of the antiapoptotic proteins Bcl-2 and Bag-1. |
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Authors:
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S Jeay; G E Sonenshein; M C Postel-Vinay; E Baixeras |
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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: Molecular endocrinology (Baltimore, Md.) Volume: 14 ISSN: 0888-8809 ISO Abbreviation: Mol. Endocrinol. Publication Date: 2000 May |
Date Detail:
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Created Date: 2000-08-10 Completed Date: 2000-08-10 Revised Date: 2007-11-14 |
Medline Journal Info:
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Nlm Unique ID: 8801431 Medline TA: Mol Endocrinol Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: 650-61 Citation Subset: IM |
Affiliation:
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INSERM Unité 344, Endocrinologie Moléculaire, Faculté de Médecine Necker, Paris, France. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Animals Apoptosis / drug effects* Autocrine Communication Carrier Proteins / biosynthesis Cattle Cell Cycle / drug effects Cell Line Culture Media / pharmacology DNA, Complementary / genetics DNA-Binding Proteins / genetics, physiology Depression, Chemical Dimerization Genes, bcl-2 Growth Hormone / antagonists & inhibitors, pharmacology* Hematopoietic Stem Cells / cytology, drug effects* I-kappa B Proteins* Interleukin-3 / pharmacology* Mice NF-kappa B / physiology* Proto-Oncogene Proteins c-bcl-2 / biosynthesis Rats Receptors, Somatotropin / drug effects*, genetics, metabolism Transcription Factors Transcription, Genetic / drug effects* Transfection bcl-X Protein |
| Grant Support | |
ID/Acronym/Agency:
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CA-36355/CA/NCI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/BCL2-associated athanogene 1 protein; 0/Bcl2l1 protein, mouse; 0/Bcl2l1 protein, rat; 0/Carrier Proteins; 0/Culture Media; 0/DNA, Complementary; 0/DNA-Binding Proteins; 0/I-kappa B Proteins; 0/Interleukin-3; 0/NF-kappa B; 0/Proto-Oncogene Proteins c-bcl-2; 0/Receptors, Somatotropin; 0/Transcription Factors; 0/bcl-X Protein; 139874-52-5/NF-kappaB inhibitor alpha; 9002-72-6/Growth Hormone |
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