ArticleMolecular neurodegeneration2010
ADAR2-dependent RNA editing of GluR2 is involved in thiamine deficiency-induced alteration of calcium dynamics.
Article in Molecular neurodegeneration, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 28 citations in OpenAlex.
- RNA editing of ion channels and receptors in physiology and neurological disorders.Oxford open neuroscience · 2022Review
- The effects of RNA editing in cancer tissue at different stages in carcinogenesis.RNA biology · 2021Review
- Article
- AMPA receptor GluA2 subunit defects are a cause of neurodevelopmental disorders.Nature communications · 2019Article
- SRSF9 selectively represses ADAR2-mediated editing of brain-specific sites in primates.Nucleic acids research · 2018Article
- mGluR5 Tunes NGF/TrkA Signaling to Orient Spiny Stellate Neuron Dendrites Toward Thalamocortical Axons During Whisker-Barrel Map Formation.Cerebral cortex (New York, N.Y. : 1991) · 2018Article
- A-to-I RNA editing in the rat brain is age-dependent, region-specific and sensitive to environmental stress across generations.BMC genomics · 2018Article
- Thiamine Deficiency and Neurodegeneration: the Interplay Among Oxidative Stress, Endoplasmic Reticulum Stress, and Autophagy.Molecular neurobiology · 2017Review
- Thiamine Deficiency Increases CaCellular and molecular neurobiology · 2017Article
- Thiamine deficiency induces endoplasmic reticulum stress and oxidative stress in human neurons derived from induced pluripotent stem cells.Toxicology and applied pharmacology · 2017Article
- Thiamine Deficiency in Tropical Pediatrics: New Insights into a Neglected but Vital Metabolic Challenge.Frontiers in nutrition · 2016Review
- Thiamine deficiency induces anorexia by inhibiting hypothalamic AMPK.Neuroscience · 2014Article
- Down-regulation of the RNA editing enzyme ADAR2 contributes to RGC death in a mouse model of glaucoma.PloS one · 2014Article
- Autophagy alleviates neurodegeneration caused by mild impairment of oxidative metabolism.Journal of neurochemistry · 2013Article
- RNA-interacting proteins act as site-specific repressors of ADAR2-mediated RNA editing and fluctuate upon neuronal stimulation.Nucleic acids research · 2013Article
- GluA2 AMPA glutamate receptor subunit exhibits codon 607 Q/R RNA editing in the lens.Biochemical and biophysical research communications · 2012Article
- Research advances at the Institute for Nutritional Sciences at Shanghai, China.Advances in nutrition (Bethesda, Md.) · 2011Review
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
Abstract
backgroundThiamine (vitamin B1) deficiency (TD) causes mild impairment of oxidative metabolism and region-selective neuronal loss in the central nervous system (CNS). TD in animals has been used to model aging-associated neurodegeneration in the brain. The mechanisms of TD-induced neuron death are complex, and it is likely multiple mechanisms interplay and contribute to the action of TD. In this study, we demonstrated that TD significantly increased intracellular calcium concentrations [Ca2+]i in cultured cortical neurons.
resultsTD drastically potentiated AMPA-triggered calcium influx and inhibited pre-mRNA editing of GluR2, a Ca2+-permeable subtype of AMPA receptors. The Ca2+ permeability of GluR2 is regulated by RNA editing at the Q/R site. Edited GluR2 (R) subunits form Ca2+-impermeable channels, whereas unedited GluR2 (Q) channels are permeable to Ca2+ flow. TD inhibited Q/R editing of GluR2 and increased the ratio of unedited GluR2. The Q/R editing of GluR2 is mediated by adenosine deaminase acting on RNA 2 (ADAR2). TD selectively decreased ADAR2 expression and its self-editing ability without affecting ADAR1 in cultured neurons and in the brain tissue. Over-expression of ADAR2 reduced AMPA-mediated rise of [Ca2+]i and protected cortical neurons against TD-induced cytotoxicity, whereas down-regulation of ADAR2 increased AMPA-elicited Ca2+ influx and exacerbated TD-induced death of cortical neurons.
conclusionsOur findings suggest that TD-induced neuronal damage may be mediated by the modulation of ADAR2-dependent RNA Editing of GluR2.
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Registered trials
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