ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2005
Role of protein phosphatases in estrogen-mediated neuroprotection.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 41 citations in OpenAlex.
- Role of serine/threonine phosphatases 1 and 2A in pancreatic acinar fluid and electrolyte secretion.American journal of physiology. Gastrointestinal and liver physiology · 2026Article
- Supraphysiologic-dose anabolic-androgenic steroid use: A risk factor for dementia?Neuroscience and biobehavioral reviews · 2019Review
- Phosphatase Actin Regulator-1 (PHACTR-1) Knockdown Suppresses Cell Proliferation and Migration and Promotes Cell Apoptosis in the bEnd.3 Mouse Brain Capillary Endothelial Cell Line.Medical science monitor : international medical journal of experimental and clinical research · 2019Article
- Alpha-Synuclein Suppresses Retinoic Acid-Induced Neuronal Differentiation by Targeting the Glycogen Synthase Kinase-3β/β-Catenin Signaling Pathway.Molecular neurobiology · 2018Article
- Isolation and identification of twelve metabolites of isocorynoxeine in rat urine and their neuroprotective activities in HT22 cell assay.Planta medica · 2015Article
- Molecular and cellular mechanism of okadaic acid (OKA)-induced neurotoxicity: a novel tool for Alzheimer's disease therapeutic application.Molecular neurobiology · 2014Review
- Urinary metabolites of isorhynchophylline in rats and their neuroprotective activities in the HT22 cell assay.Fitoterapia · 2014Article
- Alkaloids from the hook-bearing branch of Uncariarhynchophylla and their neuroprotective effects against glutamate-induced HT22 cell death.Journal of Asian natural products research · 2014Article
- Effect of okadaic acid on cultured clam heart cells: involvement of MAPkinase pathways.Biology open · 2012Article
- Long-term pioglitazone treatment improves learning and attenuates pathological markers in a mouse model of Alzheimer's disease.Journal of Alzheimer's disease : JAD · 2012Article
- Imaging of a glucose analog, calcium and NADH in neurons and astrocytes: dynamic responses to depolarization and sensitivity to pioglitazone.Cell calcium · 2011Article
- 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
- Localization of dopamine- and cAMP-regulated phosphoprotein-32 and inhibitor-1 in area 9 of Macaca mulatta prefrontal cortex.Neuroscience · 2010Article
- Role of protein phosphatases and mitochondria in the neuroprotective effects of estrogens.Frontiers in neuroendocrinology · 2009Review
- Mechanism of okadaic acid-induced neuronal death and the effect of estrogens.Journal of neurochemistry · 2009Article
- The potential for estrogens in preventing Alzheimer's disease and vascular dementia.Therapeutic advances in neurological disorders · 2009Article
- Estrogen regulation of proteins in the rat ventromedial nucleus of the hypothalamus.Journal of proteome research · 2008Article
- Protein phosphatase 1, protein phosphatase 2A, and calcineurin play a role in estrogen-mediated neuroprotection.Endocrinology · 2008Article
- Estradiol attenuates tau hyperphosphorylation induced by upregulation of protein kinase-A.Neurochemical research · 2008Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
The signaling pathways that mediate neurodegeneration are complex and involve a balance between phosphorylation and dephosphorylation of signaling and structural proteins. We have shown previously that 17beta-estradiol and its analogs are potent neuroprotectants. The purpose of this study was to delineate the role of protein phosphatases (PPs) in estrogen neuroprotection against oxidative stress and excitotoxicity. HT-22 cells, C6-glioma cells, and primary rat cortical neurons were exposed to the nonspecific serine/threonine protein phosphatase inhibitors okadaic acid and calyculin A at various concentrations in the presence or absence of 17beta-estradiol and/or glutamate. Okadaic acid and calyculin A caused a dose-dependent decrease in cell viability in HT-22, C6-glioma, and primary rat cortical neurons. 17beta-Estradiol did not show protection against neurotoxic concentrations of either okadaic acid or calyculin A in these cells. In the absence of these serine/threonine protein phosphatase inhibitors, 17beta-estradiol attenuated glutamate toxicity. However, in the presence of effective concentrations of these protein phosphatase inhibitors, 17beta-estradiol protection against glutamate toxicity was lost. Furthermore, glutamate treatment in HT-22 cells and primary rat cortical neurons caused a 50% decrease in levels of PP1, PP2A, and PP2B protein, whereas coadministration of 17beta-estradiol with glutamate prevented the decrease in PP1, PP2A, and PP2B levels. These results suggest that 17beta-estradiol may protect cells against glutamate-induced oxidative stress and excitotoxicity by activating a combination of protein phosphatases.
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