ArticleMolecular and cellular neurosciences2011
Insulin-like growth factor-I mediates neuroprotection in proteasome inhibition-induced cytotoxicity in SH-SY5Y cells.
Article in Molecular and cellular neurosciences, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
22 citing papers in PubMed, 43 citations in OpenAlex.
- Distinct In Vitro Differentiation Protocols Differentially Affect Cytotoxicity Induced by Heavy Metals in Human Neuroblastoma SH-SY5Y Cells.Biological trace element research · 2025Article
- Insulin-Like Growth Factor Binding Protein 2 Drives Neurodegeneration in Parkinson's Disease: Insights From In Vivo and In Vitro Studies.CNS neuroscience & therapeutics · 2024Article
- Neuroprotective effects of ellorarxine in neuronal models of degeneration.Frontiers in neuroscience · 2024Article
- Sucralose Targets the Insulin Signaling Pathway in the SH-SY5Y Neuroblastoma Cell Line.Metabolites · 2023Article
- The Role of Autophagy in Chemical Proteasome Inhibition Model of Retinal Degeneration.International journal of molecular sciences · 2021Article
- Genetic Pathways Involved in the Pathogenesis of Parkinson's Disease.Advances in experimental medicine and biology · 2021Article
- Regulation of Actg1 and Gsta2 is possible mechanism by which capsaicin alleviates apoptosis in cell model of 6-OHDA-induced Parkinson's disease.Bioscience reports · 2020Article
- IGF-1 protects SH-SY5Y cells against MPPEndocrine connections · 2018Article
- The Molecular Physiopathogenesis of Islet Amyloidosis.Handbook of experimental pharmacology · 2018Review
- Proteasome Stress Triggers Death of SH-SY5Y and T98G Cells via Different Cellular Mechanisms.Neurochemical research · 2017Article
- Reduction of RPT6/S8 (a Proteasome Component) and Proteasome Activity in the Cortex is Associated with Cognitive Impairment in Lewy Body Dementia.Journal of Alzheimer's disease : JAD · 2017Article
- Article
- Senescence associated secretory phenotype profile from primary lung mice fibroblasts depends on the senescence induction stimuli.Age (Dordrecht, Netherlands) · 2016Article
- N-Acetylcysteine in Combination with IGF-1 Enhances Neuroprotection against Proteasome Dysfunction-Induced Neurotoxicity in SH-SY5Y Cells.Parkinson's disease · 2016Article
- Degeneration of Dopaminergic Neurons Due to Metabolic Alterations and Parkinson's Disease.Frontiers in aging neuroscience · 2016Review
- Amyloid-beta protein clearance and degradation (ABCD) pathways and their role in Alzheimer's disease.Current Alzheimer research · 2015Article
- Approaches for neural tissue regeneration.Stem cell reviews and reports · 2014Review
- Regulation of autophagy and ubiquitinated protein accumulation by bFGF promotes functional recovery and neural protection in a rat model of spinal cord injury.Molecular neurobiology · 2013Article
- Article
- Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 5 institutions in 1 country.
Funding
Abstract
The proteasome is an enzyme complex responsible for targeted intracellular proteolysis. Alterations in proteasome-mediated protein clearance have been implicated in the pathogenesis of aging, Alzheimer's disease (AD) and Parkinson's disease (PD). In such diseases, proteasome inhibition may contribute to formation of abnormal protein aggregates, which in turn activate intracellular unfolded protein responses that cause oxidative stress and apoptosis. In this study, we investigated the protective effect of Insulin-like Growth Factor-I (IGF-1) for neural SH-SY5Y cells treated with the proteasomal inhibitor, Epoxomicin. In SH-SY5Y cells, Epoxomicin treatment results in accumulation of intracellular ubiquitinated proteins and cytochrome c release from damaged mitochondria, leading to cell death, in Epoxomicin time- and dose-dependent manner. In cells treated with small amounts of IGF-1, the same dosages of Epoxomicin reduced both mitochondrial damage (cytochrome c release) and reduced caspase-3 activation and PARP cleavage, both of which are markers of apoptosis. Notably, however, IGF-1-treated SH-SY5Y cells still contained ubiquitinated protein aggregates. This result indicates that IGF-1 blocks the downstream apoptotic consequences of Epoxomicin treatment leading to decreased proteasome function. Clues as to the mechanism for this protective effect come from (a) increased AKT phosphorylation observed in IGF-1-protected cells, vs. cells exposed to Epoxomicin without IGF-1, and (b) reduction of IGF-1 protection by pretreatment of the cells with LY294002 (an inhibitor of PI3-kinase). Together these findings suggest that activation of PI3/AKT pathways by IGF-1 is involved in IGF-1 neuroprotection against apoptosis following proteasome inhibition.
Indexed as
Identifiers
What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.