ArticleJournal of neurochemistry2009
Mechanism of okadaic acid-induced neuronal death and the effect of estrogens.
Article in Journal of neurochemistry, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 33 citations in OpenAlex.
- Salbutamol and Formoterol Attenuate Okadaic Acid-Induced Cytotoxicity in Undifferentiated PC-12 Cells: Evidence for a β2-Adrenergic Receptor-Independent Protective Component.Current issues in molecular biology · 2026Article
- Diarrhetic Shellfish Poisoning Toxins: Current Insights into Toxicity, Mechanisms, and Ecological Impacts.Marine drugs · 2025Review
- Neurosteroid enantiomers as potentially novel neurotherapeutics.Neuroscience and biobehavioral reviews · 2023Review
- A systematic review for the development of Alzheimer's disease inFrontiers in aging neuroscience · 2023Article
- Melatonin Rescues the Dendrite Collapse Induced by the Pro-Oxidant Toxin Okadaic Acid in Organotypic Cultures of Rat Hilar Hippocampus.Molecules (Basel, Switzerland) · 2020Article
- Two-photon probes for in vivo multicolor microscopy of the structure and signals of brain cells.Brain structure & function · 2018Review
- Amphetamine Neurotoxicity in PC12 Cells through the PP2A/AKT/GSK3β Pathway.Neurotoxicity research · 2018Article
- Molecular and cellular mechanism of okadaic acid (OKA)-induced neurotoxicity: a novel tool for Alzheimer's disease therapeutic application.Molecular neurobiology · 2014Review
- PPAR-γ agonist GW1929 but not antagonist GW9662 reduces TBBPA-induced neurotoxicity in primary neocortical cells.Neurotoxicity research · 2014Article
- De novo synthesized estradiol protects against methylmercury-induced neurotoxicity in cultured rat hippocampal slices.PloS one · 2013Article
- Okadaic acid induces Akt hyperphosphorylation and an oxidative stress-mediated cell death in serum starved SK-N-SH human neuroblastoma cells that are augmented by rapamycin.Neuroscience letters · 2012Article
- Bi-directional regulation of CaMKIIα phosphorylation at Thr286 by NMDA receptors in cultured cortical neurons.Journal of neurochemistry · 2012Article
- Ethanol withdrawal hastens the aging of cytochrome c oxidase.Neurobiology of aging · 2012Article
- Mitochondrial mechanisms of estrogen neuroprotection.Biochimica et biophysica acta · 2010Review
- Okadaic acid induces tau phosphorylation in SH-SY5Y cells in an estrogen-preventable manner.Brain research · 2010Article
- N-methyl-D-aspartate-stimulated ERK1/2 signaling and the transcriptional up-regulation of plasticity-related genes are developmentally regulated following in vitro neuronal maturation.Journal of neuroscience research · 2009Article
- Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens.Frontiers in neuroendocrinology · 2009Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Serine/threonine protein phosphatases are important mediators of general cellular function as well as neurodegenerative processes. We have previously shown inhibition of protein phosphatases to be as neurotoxic as glutamate-induced neuronal death but resistant to neuroprotection by estrogens. In this study, the mechanism by which phosphatase inhibition via okadaic acid (OA) induced neurotoxicity is explored. Neurons were exposed to OA or glutamate in the presence or absence of various protein kinases inhibitors, and/or one of four estrogens. Both OA and glutamate induced cell death via increased reactive oxygen species, protein carbonylation, lipid peroxidation, caspase-3 activity, and mitochondrial dysfunction. All estrogens attenuated glutamate-mediated responses, but not OA-induced responses. In addition, inhibition of protein kinase C and mitogen-activated protein kinase pathway was neuroprotective against glutamate but not OA toxicity. Interestingly, inhibition of mitogen-activated protein kinase pathway with PD98096 or U0126 caused a decrease in reactive oxygen species production suggesting that activation of ERK1/2 could further exacerbate the oxidative stress caused by glutamate-induced toxicity; however, these inhibitors had no effect on OA-induced toxicity. Collectively, these results indicate that both glutamate and OA neurotoxicities are mediated by persistent activation of ERK1/2 and/or protein kinase C and a resulting oxidative stress, and that protein phosphatase activity is an important and necessary aspect of estrogen-mediated neuroprotection.
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Registered trials
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.