Publication: Interleukin-1beta interferes with signal transduction induced by neurotrophin-3 in cortical neurons.
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Issued Date
2012
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eng
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Mahidol University
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National Institutes of Health (NIH)(available from PubMed Central (PMC))
Bibliographic Citation
Brain Res. Vol.10, No.1188 (2008), 189-197
Suggested Citation
Rungtip Soiampornkula, Tongb, Liqi, Wipawan Thangnipona, Balazsb, Robert, Cotmanb, Carl W. Interleukin-1beta interferes with signal transduction induced by neurotrophin-3 in cortical neurons.. Brain Res. Vol.10, No.1188 (2008), 189-197. Retrieved from: https://repository.li.mahidol.ac.th/handle/123456789/1843
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Title
Interleukin-1beta interferes with signal transduction induced by neurotrophin-3 in cortical neurons.
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Abstract
It was previously observed that IL-1beta interferes with BDNF-induced TrkB-mediated signal transduction and protection of cortical neurons from apoptosis evoked by deprivation from trophic support [Tong L., Balazs R., Soiampornkul R., Thangnipon W., Cotman C.W., 2007. Interleukin-1beta impairs brain derived neurotrophic factor-induced signal transduction. Neurobiol. Aging]. Here we investigated whether the effect of the cytokine on neurotrophin signaling is more general. The influence of IL-1beta on NT-3 signaling was therefore studied under conditions when NT-3 primarily activated the TrkC receptor. The cytokine reduced NT-3-induced activation of MAPK/ERK and Akt, but did not interfere with Trk receptor autophosphorylation. IL-1beta reduced tyrosine phosphorylation of the docking proteins, IRS-1 and Shc, which convey receptor activation to the downstream protein kinase cascades. These are the steps that are also inhibited by IL-1beta in BDNF-induced signal transduction. The functional consequences of the effect of IL-1beta on NT-3 signaling were severe, as NT-3 protection of the trophic support-deprived cortical neurons was abrogated. In view of the role in the maintenance and plasticity of neurons of ERK, Akt and CREB, which are activated by neurotrophins, elevated IL-1beta levels in the brain in Alzheimer's disease and other neurodegenerative diseases might contribute to the decline in cognitive functions before the pathological signs of the disease develop.