Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis - PubMed (original) (raw)
Tumor necrosis factors protect neurons against metabolic-excitotoxic insults and promote maintenance of calcium homeostasis
B Cheng et al. Neuron. 1994 Jan.
Abstract
Emerging data indicate that neurotrophic factors and cytokines utilize similar signal transduction mechanisms. Although neurotrophic factors can protect CNS neurons against a variety of insults, the role of cytokines in the injury response is unclear. We now report that TNF beta and TNF alpha (1-100 ng/ml) can protect cultured embryonic rat hippocampal, septal, and cortical neurons against glucose deprivation-induced injury and excitatory amino acid toxicity. The elevation of intracellular calcium concentration ([Ca2+]i) induced by glucose deprivation, glutamate, NMDA, or AMPA was attenuated in neurons pretreated with TNF beta. The mechanism whereby TNFs stabilize [Ca2+]i may involve regulation of the expression of proteins involved in maintaining [Ca2+]i homeostasis, since both TNF beta and TNF alpha caused a 4- to 8-fold increase in the number of neurons expressing the calcium-binding protein calbindin-D28k. These data suggest a neuroprotective role for TNFs in the brain's response to injury.
Similar articles
- Tumor necrosis factors alpha and beta protect neurons against amyloid beta-peptide toxicity: evidence for involvement of a kappa B-binding factor and attenuation of peroxide and Ca2+ accumulation.
Barger SW, Hörster D, Furukawa K, Goodman Y, Krieglstein J, Mattson MP. Barger SW, et al. Proc Natl Acad Sci U S A. 1995 Sep 26;92(20):9328-32. doi: 10.1073/pnas.92.20.9328. Proc Natl Acad Sci U S A. 1995. PMID: 7568127 Free PMC article. - Calcium and glutamate-induced cortical neuronal death.
Choi DW, Hartley DM. Choi DW, et al. Res Publ Assoc Res Nerv Ment Dis. 1993;71:23-34. Res Publ Assoc Res Nerv Ment Dis. 1993. PMID: 8093332 Review. No abstract available. - Altered calcium signaling and neuronal injury: stroke and Alzheimer's disease as examples.
Mattson MP, Rydel RE, Lieberburg I, Smith-Swintosky VL. Mattson MP, et al. Ann N Y Acad Sci. 1993 May 28;679:1-21. doi: 10.1111/j.1749-6632.1993.tb18285.x. Ann N Y Acad Sci. 1993. PMID: 8512177 Review.
Cited by
- Chronic neuron- and age-selective down-regulation of TNF receptor expression in triple-transgenic Alzheimer disease mice leads to significant modulation of amyloid- and Tau-related pathologies.
Montgomery SL, Narrow WC, Mastrangelo MA, Olschowka JA, O'Banion MK, Bowers WJ. Montgomery SL, et al. Am J Pathol. 2013 Jun;182(6):2285-97. doi: 10.1016/j.ajpath.2013.02.030. Epub 2013 Apr 6. Am J Pathol. 2013. PMID: 23567638 Free PMC article. - Excitotoxic and excitoprotective mechanisms: abundant targets for the prevention and treatment of neurodegenerative disorders.
Mattson MP. Mattson MP. Neuromolecular Med. 2003;3(2):65-94. doi: 10.1385/NMM:3:2:65. Neuromolecular Med. 2003. PMID: 12728191 Review. - TNF-alpha and TNF-beta gene polymorphisms in cerebral infarction.
Um JY, An NH, Kim HM. Um JY, et al. J Mol Neurosci. 2003;21(2):167-71. doi: 10.1385/JMN:21:2:167. J Mol Neurosci. 2003. PMID: 14593215 - Glucocorticoids and central nervous system inflammation.
Dinkel K, Ogle WO, Sapolsky RM. Dinkel K, et al. J Neurovirol. 2002 Dec;8(6):513-28. doi: 10.1080/13550280290100914. J Neurovirol. 2002. PMID: 12476346 Review. - The induction of the TNFalpha death domain signaling pathway in Alzheimer's disease brain.
Zhao M, Cribbs DH, Anderson AJ, Cummings BJ, Su JH, Wasserman AJ, Cotman CW. Zhao M, et al. Neurochem Res. 2003 Feb;28(2):307-18. doi: 10.1023/a:1022337519035. Neurochem Res. 2003. PMID: 12608703
Publication types
MeSH terms
Substances
LinkOut - more resources
Full Text Sources
Miscellaneous