ArticleCell stress & chaperones2013
Induction of heat shock proteins in cerebral cortical cultures by celastrol.
Article in Cell stress & chaperones, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Protein painting reveals pervasive remodeling of conserved proteostasis machinery in response to pharmacological stimuli.NPJ systems biology and applications · 2022Article
- Neuroprotective Effects of Celastrol in Neurodegenerative Diseases-Unscramble Its Major Mechanisms of Action and Targets.Aging and disease · 2022Review
- The therapeutic potential of triptolide and celastrol in neurological diseases.Frontiers in pharmacology · 2022Review
- Indolyl- and Pyrrolylazine Derivatives Cause the Accumulation of Heat Shock Protein Hsp70 in Sh-Sy5Y Human Neuroblastoma Cells.Doklady. Biochemistry and biophysics · 2020Article
- Heat shock protein 90 inhibition and multi-target approach to maximize cardioprotection in ischaemic injury.British journal of pharmacology · 2020Review
- Brain Transcriptome Analysis Links Deficiencies of Stress-Responsive Proteins to the Pathomechanism of Kii ALS/PDC.Antioxidants (Basel, Switzerland) · 2020Article
- Pyrrolylquinoxaline-2-One Derivative as a Potent Therapeutic Factor for Brain Trauma Rehabilitation.Pharmaceutics · 2020Article
- Natural Products as Modulators of the Proteostasis Machinery: Implications in Neurodegenerative Diseases.International journal of molecular sciences · 2019Review
- Neurodegenerative Diseases: Regenerative Mechanisms and Novel Therapeutic Approaches.Brain sciences · 2018Review
- Heat Shock Proteins in Alzheimer's Disease: Role and Targeting.International journal of molecular sciences · 2018Review
- Celastrol: A Spectrum of Treatment Opportunities in Chronic Diseases.Frontiers in medicine · 2017Review
- Daphnetin protects oxidative stress-induced neuronal apoptosis via regulation of MAPK signaling and HSP70 expression.Oncology letters · 2016Article
- Celastrol protects ischaemic myocardium through a heat shock response with up-regulation of haeme oxygenase-1.British journal of pharmacology · 2014Article
- Localization of heat shock proteins in cerebral cortical cultures following induction by celastrol.Cell stress & chaperones · 2014Article
- Stress-induced localization of HSPA6 (HSP70B') and HSPA1A (HSP70-1) proteins to centrioles in human neuronal cells.Cell stress & chaperones · 2014Article
- Alcohol stress, membranes, and chaperones.Cell stress & chaperones · 2014Review
- Peptide deformylase inhibitor actinonin reduces celastrol's HSP70 induction while synergizing proliferation inhibition in tumor cells.BMC cancer · 2014Article
- Article
- Heat shock protein 70 in Alzheimer's disease.BioMed research international · 2014Review
- ER stress-mediated apoptosis induced by celastrol in cancer cells and important role of glycogen synthase kinase-3β in the signal network.Cell death & disease · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease, Parkinson's disease and amyotrophic lateral sclerosis (ALS) are 'protein misfolding disorders' of the mature nervous system that are characterized by the accumulation of protein aggregates and selective cell loss. Different brain regions are impacted, with Alzheimer's affecting cells in the cerebral cortex, Parkinson's targeting dopaminergic cells in the substantia nigra and ALS causing degeneration of cells in the spinal cord. These diseases differ widely in frequency in the human population. Alzheimer's is more frequent than Parkinson's and ALS. Heat shock proteins (Hsps) are 'protein repair agents' that provide a line of defense against misfolded, aggregation-prone proteins. We have suggested that differing levels of constitutively expressed Hsps (Hsc70 and Hsp27) in neural cell populations confer a variable buffering capacity against 'protein misfolding disorders' that correlates with the relative frequencies of these neurodegenerative diseases. The high relative frequency of Alzheimer's may due to low levels of Hsc70 and Hsp27 in affected cell populations that results in a reduced defense capacity against protein misfolding. Here, we demonstrate that celastrol, but not classical heat shock treatment, is effective in inducing a set of neuroprotective Hsps in cultures derived from cerebral cortices, including Hsp70, Hsp27 and Hsp32. This set of Hsps is induced by celastrol at 'days in vitro' (DIV) 13 when cultured cortical cells reached maturity. The inducibility of a set of neuroprotective Hsps in mature cortical cultures at DIV13 suggests that celastrol is a potential agent to counter Alzheimer's disease, a neurodegenerative 'protein misfolding disorder' of the adult brain that targets cells in the cerebral cortex.
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