ArticleMolecular neurobiology2017
Trehalose Inhibits Protein Aggregation Caused by Transient Ischemic Insults Through Preservation of Proteasome Activity, Not via Induction of Autophagy.
Article in Molecular neurobiology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 36 citations in OpenAlex.
- Trehalose's untapped mechanisms in alzheimer's: gut-brain-autophagy signalling beyond the usual targets.Daru : journal of Faculty of Pharmacy, Tehran University of Medical Sciences · 2026Review
- Mechanistic exploration of ubiquitination-mediated pathways in cerebral ischemic injury.Molecular biology reports · 2024Review
- Trehalose Promotes Clearance of Proteotoxic Aggregation of Neurodegenerative Disease-Associated Aberrant Proteins.Molecular neurobiology · 2024Article
- Article
- Protein Aggregation in the Pathogenesis of Ischemic Stroke.Cellular and molecular neurobiology · 2021Review
- Associations between Huwe1 and autophagy in rat cerebral neuron oxygen‑glucose deprivation and reperfusion injury.Molecular medicine reports · 2020Article
- Trehalose for Ocular Surface Health.Biomolecules · 2020Review
- Article
- The Role of Ubiquitin-Proteasome Pathway and Autophagy-Lysosome Pathway in Cerebral Ischemia.Oxidative medicine and cellular longevity · 2020Review
- Autophagy induction by trehalose: Molecular mechanisms and therapeutic impacts.Journal of cellular physiology · 2018Review
- Mechanism of neuroprotection by trehalose: controversy surrounding autophagy induction.Cell death & disease · 2018Review
- Protein Modifications with Ubiquitin as Response to Cerebral Ischemia-Reperfusion Injury.Translational stroke research · 2018Review
- Trehalose inhibits HInternational journal of medical sciences · 2018Article
- Trehalose Activates Autophagy and Prevents Hydrogen Peroxide-Induced Apoptosis in the Bone Marrow Stromal Cells.Iranian journal of pharmaceutical research : IJPR · 2018Article
- Endoplasmic reticulum stress regulates oxygen-glucose deprivation-induced parthanatos in human SH-SY5Y cells via improvement of intracellular ROS.CNS neuroscience & therapeutics · 2018Article
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
Protein aggregation has been proved to be a pathological basis accounting for neuronal death caused by either transient global ischemia or oxygen glucose deprivation (OGD), and inhibition of protein aggregation is emerging as a potential strategy of preventing brain damage. Trehalose was found to inhibit protein aggregation caused by neurodegenerative diseases via induction of autophagy, whereas its effect is still elusive on ischemia-induced protein aggregation. In this study, we investigated this issue by using rat model of transient global ischemia and SH-SY5Y model of OGD. We found that pretreatment with trehalose inhibited transient global ischemia-induced neuronal death in the hippocampus CA1 neurons and OGD-induced death in SH-SY5Y cells, which was associated with inhibition of the formation of ubiquitin-labeled protein aggregates and preservation of proteasome activity. In vitro study showed that the protection of trehalose against OGD-induced cell death and protein aggregation in SH-SY5Y cells was reversed when proteasome activity was inhibited by MG-132. Further studies revealed that trehalose prevented OGD-induced reduction of proteasome activity via suppression of both oxidative stress and endoplasmic reticulum stress. Particularly, our results showed that trehalose inhibited OGD-induced autophagy. Therefore, we demonstrated that proteasome dysfunction contributed to protein aggregation caused by ischemic insults and trehalose prevented protein aggregation via preservation of proteasome activity, not via induction of autophagy.
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