ArticleCellular and molecular neurobiology2008
Inactivation of glycogen synthase kinase-3beta and up-regulation of LINGO-1 are involved in LINGO-1 antagonist regulated survival of cerebellar granular neurons.
Article in Cellular and molecular neurobiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 21 citations in OpenAlex.
- Genetic Risk Factors for Essential Tremor: A Review.Tremor and other hyperkinetic movements (New York, N.Y.) · 2020Review
- Soluble Nogo receptor 1 fusion protein protects neural progenitor cells in rats with ischemic stroke.Neural regeneration research · 2019Article
- LINGO-1 receptor promotes neuronal apoptosis by inhibiting WNK3 kinase activity.The Journal of biological chemistry · 2013Article
- Amino-Nogo-A antagonizes reactive oxygen species generation and protects immature primary cortical neurons from oxidative toxicity.Cell death and differentiation · 2012Article
- LINGO-1 and Neurodegeneration: Pathophysiologic Clues for Essential Tremor.Tremor and other hyperkinetic movements (New York, N.Y.) · 2012Article
- Linking oligodendrocyte and myelin dysfunction to neurocircuitry abnormalities in schizophrenia.Progress in neurobiology · 2011Review
- Neurotrophin roles in retinal ganglion cell survival: lessons from rat glaucoma models.Experimental eye research · 2009Review
- Variant in the sequence of the LINGO1 gene confers risk of essential tremor.Nature genetics · 2009Article
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
LINGO-1 has been critically implicated in the central regulation of CNS axon regeneration and oligodendrocyte maturation. We have recently demonstrated that pretreatment with LINGO-1 antagonist (LINGO-1-Fc) inhibited low potassium-induced cerebellar granular neurons (CGNs) apoptosis. In the present study, we examined the neuroprotective mechanism of LINGO-1-Fc by Western blot and in situ GST pull-down assay. CGN cultures were preincubated in medium with LINGO-1-Fc or control protein at the concentration of 10 mug/ml for 2 h and then switched to low potassium medium in the presence of corresponding proteins. Cultures were harvested at indicated time intervals for successive analysis. Several apoptosis-associated signaling factors, GSK-3beta, ERK1/2, and Rho GTPases, were observed to be activated in response to potassium deprivation and the activation/dephosphorylation of GSK-3beta was suppressed by LINGO-1-Fc pretreatment compared with control group. Besides, the endogenous LINGO-1 expression level of CGN cultures was augmented by low potassium stimuli and restrained by LINGO-1 antagonist treatment. Although the protein level of p75(NTR) and Nogo-A were down-regulated in different patterns during apoptosis, neither of them was affected by LINGO-1-Fc application. Taken together, these results suggest a new mechanism of LINGO-1 antagonist regulated neuronal survival involving protein synthesis of LINGO-1 and inactivation of GSK-3 pathway.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.