Induction of Oxidative Stress in SH-SY5Y Cells by Overexpression of hTau40 and Its Mitigation by Redox-Active Nanoparticles.
Natalia PieńkowskaMargaret FahnestockCrystal MahadeoIzabela ZaborniakPaweł ChmielarzGrzegorz BartoszIzabela Sadowska-BartoszPublished in: International journal of molecular sciences (2022)
Abnormally phosphorylated tau protein is the principal component of neurofibrillary tangles, accumulating in the brain in many neurodegenerative diseases, including Alzheimer's disease. The aim of this study was to examine whether overexpression of tau protein leads to changes in the redox status of human neuroblastoma SH-SY5Y cells. The level of reactive oxygen species (ROS) was elevated in tau-overexpressing cells (TAU cells) as compared with cells transfected with the empty vector (EP cells). The level of glutathione was increased in TAU cells, apparently due to overproduction as an adaptation to oxidative stress. The TAU cells had elevated mitochondrial mass. They were more sensitive to 6-hydroxydopamine, delphinidin, 4-amino-TEMPO, and nitroxide-containing nanoparticles (NPs) compared to EP controls. These results indicate that overexpression of the tau protein imposes oxidative stress on the cells. The nitroxide 4-amino-TEMPO and nitroxide-containing nanoparticles (NPs) mitigated oxidative stress in TAU cells, decreasing the level of ROS. Nitroxide-containing nanoparticles lowered the level of lipid peroxidation in both TAU and EP cells, suggesting that nitroxides and NPs may mitigate tau-protein-induced oxidative stress.
Keyphrases
- induced apoptosis
- oxidative stress
- cell cycle arrest
- endoplasmic reticulum stress
- cell death
- signaling pathway
- reactive oxygen species
- cerebrospinal fluid
- endothelial cells
- cell proliferation
- small molecule
- climate change
- pi k akt
- transcription factor
- hydrogen peroxide
- mild cognitive impairment
- protein protein
- subarachnoid hemorrhage
- cerebral ischemia