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Decrease of Tau hyperphosphorylation by 17β estradiol requires sphingosine kinase in a glutamate toxicity model.

Alejandro Lopez-Tobón¹, Efraín Cepeda-Prado, Gloria Patricia Cardona-Gómez

¹Group of Neuroscience of Antioquia, Cellular and Molecular Neurobiology Area, School of Medicine, SIU, University of Antioquia, Street 62 # 52-59; Tower 1, Floor 4th, Laboratory 411-412, Medellín, Colombia.

Neurochemical Research

|June 23, 2009

Summary

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17β-estradiol (E2) protects against glutamate toxicity in nerve cells. This neuroprotective effect against Tau hyperphosphorylation by E2 requires sphingosine kinase (SphK) activity.

Area of Science:

Neuroscience
Cell Biology
Biochemistry

Background:

Estrogens are linked to sphingosine kinase (SphK) activity, which synthesizes sphingosine-1-phosphate (S-1P).
The interaction between estrogens and SphK in the nervous system remains largely undocumented.
Glutamate toxicity is a significant concern in neurological disorders.

Purpose of the Study:

To investigate the effect of SphK inhibition on the neuroprotective properties of 17β-estradiol (E2) against glutamate toxicity.
To elucidate the role of SphK in E2-mediated protection, particularly concerning Tau hyperphosphorylation.

Main Methods:

A glutamate toxicity model was established using SH-SY5Y neuroblastoma cells.
Cells were pre-treated with 17β-estradiol (E2) and/or SphK inhibitors.

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Evaluated effects included cytoskeletal actin changes, nuclear fragmentation, Tau hyperphosphorylation, and p25/p35 cleavage.

Main Results:

Glutamate induced significant cytotoxic stress, including actin changes, nuclear fragmentation, and Tau hyperphosphorylation.
17β-estradiol (E2) pre-treatment effectively prevented these glutamate-induced effects.
SphK inhibition did not abolish E2's protective effect but exacerbated glutamate-induced Tau hyperphosphorylation, an effect not reversed by E2.

Conclusions:

17β-estradiol (E2) demonstrates neuroprotective capabilities against glutamate toxicity in SH-SY5Y cells.
The protective mechanism of E2 against glutamate-induced Tau hyperphosphorylation is dependent on sphingosine kinase (SphK) activity.
SphK plays a critical role in modulating Tau pathology in the context of estrogen signaling and excitotoxicity.