TNFa mediates Schwann cell death by upregulating p75NTR expression without sustained activation of NFkB

Boyle, K, Azari, M, Cheema, S and Petratos, S 2005, 'TNFa mediates Schwann cell death by upregulating p75NTR expression without sustained activation of NFkB', Neurobiology of Disease, vol. 20, no. 2, pp. 412-427.


Document type: Journal Article
Collection: Journal Articles

Title TNFa mediates Schwann cell death by upregulating p75NTR expression without sustained activation of NFkB
Author(s) Boyle, K
Azari, M
Cheema, S
Petratos, S
Year 2005
Journal name Neurobiology of Disease
Volume number 20
Issue number 2
Start page 412
End page 427
Total pages 16
Publisher Academic Press
Abstract Administration of tumour necrosis factor a (TNFa) to axotomised mouse neonatal sciatic nerves increased Schwann cell apoptosis in the distal nerve segments, 5-fold greater than axotomy alone. TNFa upregulated the low affinity neurotrophin receptor, p75NTR, indicative of phenotype reversion in Schwann cells. Furthermore, re-expression of p75NTR and downregulation of the pro-myelinating transcription factor, Oct 6, in Schwann cells occurred by treatment with TNFa, even after the maturation of these cells with brain derived neurotrophic factor (BDNF). TNFa treatment of Schwann cells produced only a transient activation of NF?B. More importantly, in NF?B (p65) mutant mice, axotomy increased Schwann cell apoptosis further than that seen in mice expressing NF?B (p65), implicating a survival role for NF?B. Collectively, these data suggest that TNFa can potentiate Schwann cell death through the modulation of their phenotype. Immature Schwann cells express a high level of p75 NTR and as a consequence are susceptible to extracellular death stimuli because of the lack of sustained NF?B translocation.
Subject Clinical Sciences not elsewhere classified
DOI - identifier 10.1016/j.nbd.2005.03.022
ISSN 0969-9961
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