ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
The systemic amyloid precursor transthyretin (TTR) behaves as a neuronal stress protein regulated by HSF1 in SH-SY5Y human neuroblastoma cells and APP23 Alzheimer's disease model mice.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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Who cites it
29 citing papers in PubMed, 53 citations in OpenAlex.
- Spatial transcriptomics reveals an unexpected impact of tau and tau pathology on the expression of transthyretin.Frontiers in aging neuroscience · 2025Article
- Gene expression of Decompression Sickness-resistant rats through a miRnome/transcriptome crossed approach.Communications biology · 2024Article
- Multi-transcriptomics reveals brain cellular responses to peripheral infection in Alzheimer's disease model mice.Cell reports · 2023Article
- Neuroprotective Effects of Celastrol in Neurodegenerative Diseases-Unscramble Its Major Mechanisms of Action and Targets.Aging and disease · 2022Review
- Stress-responsive regulation of extracellular proteostasis.The Journal of cell biology · 2022Review
- Chaperones mainly suppress primary nucleation during formation of functional amyloid required for bacterial biofilm formation.Chemical science · 2022Article
- Concurrent cardiac transthyretin and brain β amyloid accumulation among the older adults: The Hisayama study.Brain pathology (Zurich, Switzerland) · 2022Article
- Transthyretin as a Biomarker to Predict and Monitor Major Depressive Disorder Identified by Whole-Genome Transcriptomic Analysis in Mouse Models.Biomedicines · 2021Article
- Review
- Serum proteomic analysis of novel predictive serum proteins for neurological prognosis following cardiac arrest.Journal of cellular and molecular medicine · 2021Article
- Is pseudoexfoliation glaucoma a neurodegenerative disorder?Journal of biosciences · 2021Review
- Undiscovered Roles for Transthyretin: From a Transporter Protein to a New Therapeutic Target for Alzheimer's Disease.International journal of molecular sciences · 2020Review
- Transthyretin Inhibits Primary and Secondary Nucleations of Amyloid-β Peptide Aggregation and Reduces the Toxicity of Its Oligomers.Biomacromolecules · 2020Article
- Transthyretin expression in the postischemic brain.PloS one · 2019Article
- Accurate, strong, and stable reporting of choroid plexus epithelial cells in transgenic mice using a human transthyretin BAC.Fluids and barriers of the CNS · 2018Article
- Age-dependent cognitive dysfunction in untreated hereditary transthyretin amyloidosis.Journal of neurology · 2018Article
- A CNS-permeable Hsp90 inhibitor rescues synaptic dysfunction and memory loss in APP-overexpressing Alzheimer's mouse model via an HSF1-mediated mechanism.Molecular psychiatry · 2017Article
- Transthyretin and BRICHOS: The Paradox of Amyloidogenic Proteins with Anti-Amyloidogenic Activity for Aβ in the Central Nervous System.Frontiers in neuroscience · 2017Review
- Molecular Chaperone Accumulation in Cancer and Decrease in Alzheimer's Disease: The Potential Roles of HSF1.Frontiers in neuroscience · 2017Review
- Sex-specific hippocampal 5-hydroxymethylcytosine is disrupted in response to acute stress.Neurobiology of disease · 2016Article
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Increased neuronal synthesis of transthyretin (TTR) may favorably impact on Alzheimer's disease (AD) because TTR has been shown to inhibit Aβ aggregation and detoxify cell-damaging conformers. The mechanism whereby hippocampal and cortical neurons from AD patients and APP23 AD model mice produce more TTR is unknown. We now show that TTR expression in SH-SY5Y human neuroblastoma cells, primary hippocampal neurons and the hippocampus of APP23 mice, is significantly enhanced by heat shock factor 1 (HSF1). Chromatin immunoprecipitation (ChIP) assays demonstrated occupation of TTR promoter heat shock elements by HSF1 in APP23 hippocampi, primary murine hippocampal neurons, and SH-SY5Y cells, but not in mouse liver, cultured human hepatoma (HepG2) cells, or AC16 cultured human cardiomyocytes. Treating SH-SY5Y human neuroblastoma cells with heat shock or the HSF1 stimulator celastrol increased TTR transcription in parallel with that of HSP40, HSP70, and HSP90. With both treatments, ChIP showed increased occupancy of heat shock elements in the TTR promoter by HSF1. In vivo celastrol increased the HSF1 ChIP signal in hippocampus but not in liver. Transfection of a human HSF1 construct into SH-SY5Y cells increased TTR transcription and protein production, which could be blocked by shHSF1 antisense. The effect is neuron specific. In cultured HepG2 cells, HSF1 was either suppressive or had no effect on TTR expression confirming the differential effects of HSF1 on TTR transcription in different cell types.
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