Document Detail


Expression of the 75 kDA TNF receptor and its role in contact-mediated neuronal cell death.
MedLine Citation:
PMID:  9813268     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
We previously demonstrated TNF toxicity, at high TNF doses or in the presence of actinomycin D, in the N1E-115 neuronal cell line (N1Es), which expresses only the 55 kDa TNF receptor (TNFR). To determine whether presence of the 75 kDa TNFR increases N1E sensitivity to TNF toxicity, cells were transfected with a 75 kDa TNFR expression construct. However, 75 kDa TNFR protein expression was undetectable in stably transfected N1Es. Further investigation revealed endogenous membrane-associated TNF in this neuronal line. Co-transfection with beta-galactosidase and the 75 kDa TNFR or empty vector (pcDNA3) indicated cell loss in the 75 kDa TNFR-transfected population relative to vector-transfected populations, while inhibition of membrane-associated TNF with a neutralizing antibody led to increased 75 kDa TNFR expression in transiently transfected N1Es. We conclude that neutralization of membrane-associated TNF inhibits its interaction with the introduced 75 kDa TNFR, increasing neuronal survival and promoting 75 kDa TNFR expression. Induced 75 kDa TNFR expression in the presence of membrane-associated TNF and the 55 kDa TNFR results in lymphocyte cell death [J.K. Lazdins, M. Grell, M.R. Walker, K. Woods-Cook, P. Scheurich, K. Pfizenmaier, Membrane tumor necrosis factor (TNF) induced cooperative signaling of the TNFR60 and TNFR80 favors induction of cell death rather than virus production in HIV-infected T cells, J. Exp. Med. 185 (1997) 81-90]. This report demonstrates that membrane-associated TNF and the 75 kDa TNFR similarly contribute to neuronal cell death.
Authors:
K J Sipe; R Dantzer; K W Kelley; J A Weyhenmeyer
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, Non-P.H.S.; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Brain research. Molecular brain research     Volume:  62     ISSN:  0169-328X     ISO Abbreviation:  Brain Res. Mol. Brain Res.     Publication Date:  1998 Nov 
Date Detail:
Created Date:  1999-02-18     Completed Date:  1999-02-18     Revised Date:  2007-11-14    
Medline Journal Info:
Nlm Unique ID:  8908640     Medline TA:  Brain Res Mol Brain Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  111-21     Citation Subset:  IM    
Copyright Information:
Copyright 1998 Elsevier Science B.V.
Affiliation:
Department of Anatomy and Neurobiology, University of Kentucky, MN-224 Chandler Medical Center, 800 Rose St., Lexington, KY 40536-0298, USA. kjsipe0@staff.uiuc.edu
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MeSH Terms
Descriptor/Qualifier:
Animals
Antigens, CD / biosynthesis,  genetics,  physiology*
Apoptosis / physiology*
COS Cells
Cell Communication
Fibroblasts
Gene Expression
Neoplasm Proteins / physiology
Nerve Tissue Proteins / biosynthesis,  genetics,  physiology*
Neuroblastoma / pathology
Neurons / cytology*,  pathology
Receptors, Tumor Necrosis Factor / biosynthesis,  genetics,  physiology*
Receptors, Tumor Necrosis Factor, Type II
Recombinant Fusion Proteins / biosynthesis
Reverse Transcriptase Polymerase Chain Reaction
Transfection
Tumor Cells, Cultured
Tumor Necrosis Factor-alpha / physiology*
Grant Support
ID/Acronym/Agency:
DK49311/DK/NIDDK NIH HHS
Chemical
Reg. No./Substance:
0/Antigens, CD; 0/Neoplasm Proteins; 0/Nerve Tissue Proteins; 0/Receptors, Tumor Necrosis Factor; 0/Receptors, Tumor Necrosis Factor, Type II; 0/Recombinant Fusion Proteins; 0/Tumor Necrosis Factor-alpha

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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