Preprint Article Version 1 Preserved in Portico This version is not peer-reviewed

Geranylgeranyl Acetone Prevents Glutamate-induced Cell Death in HT-22 Cells by Increasing Mitochondrial Membrane Potential

Eriko Sugano
,
Yuka Endo
,
Akihisa Sugai
,
Yuki Kikuchi
,
Kitako Tabata
,
Taku Ozaki
,
Takahiro Kurose
,
Yoshihiro Takai
,
Yoko Mitsuguchi
,
Yoichi Honma
,
Hiroshi Tomita
*
Version 1 : Received: 3 February 2020 / Approved: 4 February 2020 / Online: 4 February 2020 (10:24:57 CET)

How to cite: Sugano, E.; Endo, Y.; Sugai, A.; Kikuchi, Y.; Tabata, K.; Ozaki, T.; Kurose, T.; Takai, Y.; Mitsuguchi, Y.; Honma, Y.; Tomita, H. Geranylgeranyl Acetone Prevents Glutamate-induced Cell Death in HT-22 Cells by Increasing Mitochondrial Membrane Potential. Preprints 2020, 2020020041. https://doi.org/10.20944/preprints202002.0041.v1 Sugano, E.; Endo, Y.; Sugai, A.; Kikuchi, Y.; Tabata, K.; Ozaki, T.; Kurose, T.; Takai, Y.; Mitsuguchi, Y.; Honma, Y.; Tomita, H. Geranylgeranyl Acetone Prevents Glutamate-induced Cell Death in HT-22 Cells by Increasing Mitochondrial Membrane Potential. Preprints 2020, 2020020041. https://doi.org/10.20944/preprints202002.0041.v1

Abstract

Geranylgeranyl acetone (GGA) protects against various types of cell damages by upregulating heat shock proteins. We investigated whether GGA protect neuronal cells from cell death induced by oxidative stress. Glutamate exposure was lethal to HT-22 cells which comprise a neuronal line derived from mouse hippocampus. This configuration is often used as a model for hippocampus neurodegeneration in vitro. In the present study, GGA protected HT-22 cells from glutamate-induced oxidative stress. GGA pretreatment did not induce Hsps. Moreover, reactive oxygen species increased to the same extent in both GGA-pretreated and untreated cells exposed to glutamate. In contrast, glutamate exposure and GGA pretreatment increased mitochondrial membrane potential. However, increases in intracellular Ca2+ concentration were inhibited by GGA pretreatment. In addition, the increase of phosphorylated ERKs by the glutamate exposure was inhibited by GGA pretreatment. These findings suggest that GGA protects HT-22 cells from glutamate-provoked cell death without Hsp induction and that the mitochondrial calcium buffering capacity plays an important role in this protective effect.

Keywords

geranylgeranyl acetone (GGA); heat shock proteins (Hsps); HT-22 (hippocampal neuronal) cells; mitochondrial membrane potentials

Subject

Medicine and Pharmacology, Pharmacology and Toxicology

Copyright: This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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