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- W2011506501 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 17β-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 17β-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. 17β-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, 17β-estradiol attenuated glutamate toxicity. However, in the presence of effective concentrations of these protein phosphatase inhibitors, 17β-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 17β-estradiol with glutamate prevented the decrease in PP1, PP2A, and PP2B levels. These results suggest that 17β-estradiol may protect cells against glutamate-induced oxidative stress and excitotoxicity by activating a combination of protein phosphatases." @default.
- W2011506501 created "2016-06-24" @default.
- W2011506501 creator A5004996901 @default.
- W2011506501 creator A5024146315 @default.
- W2011506501 creator A5038809086 @default.
- W2011506501 creator A5041649274 @default.
- W2011506501 date "2005-08-03" @default.
- W2011506501 modified "2023-09-25" @default.
- W2011506501 title "Role of Protein Phosphatases in Estrogen-Mediated Neuroprotection" @default.
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- W2011506501 doi "https://doi.org/10.1523/jneurosci.1328-05.2005" @default.
- W2011506501 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6725236" @default.