Geranylgeranyl Acetone Prevents Glutamate-induced Cell Death in HT-22 Cells by Increasing Mitochondrial Membrane Potential
| Autor: | Taku Ozaki, Yuki Kikuchi, Hiroshi Tomita, Yoichi Honma, Kitako Tabata, Eriko Sugano, Yoshihiro Takai, Yoko Mitsuguchi, Takahiro Kurose, Akihisa Sugai, Yuka Endo |
|---|---|
| Jazyk: | angličtina |
| Rok vydání: | 2020 |
| Předmět: |
0301 basic medicine
Programmed cell death Calcium buffering Glutamic Acid medicine.disease_cause Hippocampus Cell Line pharmacology_toxicology Mice 03 medical and health sciences 0302 clinical medicine Heat shock protein medicine Animals HSP70 Heat-Shock Proteins HSP90 Heat-Shock Proteins Phosphorylation Extracellular Signal-Regulated MAP Kinases Membrane Potential Mitochondrial Neurons Pharmacology chemistry.chemical_classification Membrane potential Reactive oxygen species Cell Death Chemistry Glutamate receptor Mitochondria Cell biology Oxidative Stress Neuroprotective Agents 030104 developmental biology Calcium Diterpenes Reactive Oxygen Species 030217 neurology & neurosurgery Intracellular Oxidative stress |
| Popis: | Geranylgeranyl acetone (GGA) protects against various types of cell damages by upregulating heat shock proteins. We investigated whether GGA protects 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 heat shock proteins (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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|