ArticleJournal of cellular and molecular medicine2011
Early defect of transforming growth factor β1 formation in Huntington's disease.
Article in Journal of cellular and molecular medicine, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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Who cites it
41 citing papers in PubMed, 72 citations in OpenAlex.
- Clinical-Grade Human Induced Pluripotent Stem Cell-Derived Neural Precursor Cells Restore Motor Function and Preserve Striatal Integrity in a Quinolinic Acid-Lesioned Rat Model of Huntington's Disease.Cell proliferation · 2026Article
- Oligodendroglial Mutant Huntingtin Contributes to Neuroinflammation in Huntington's Disease Mice.Neuroscience bulletin · 2026Article
- Distinct molecular patterns in R6/2 HD mouse brain: Insights from spatiotemporal transcriptomics.Neuron · 2025Article
- Cerulenin partially corrects the disrupted developmental transcriptomic signature in Huntington's disease striatal medium spiny neurons.Stem cells (Dayton, Ohio) · 2025Article
- Exploring potential developmental origins of common neurodegenerative disorders.Biochemical Society transactions · 2024Review
- Adult microglial TGFβ1 is required for microglia homeostasis via an autocrine mechanism to maintain cognitive function in mice.Nature communications · 2024Article
- Interleukin-6 as a marker of Huntington's disease progression: Systematic review and meta-analysis.Brain, behavior, & immunity - health · 2023Review
- The updated development of blood-based biomarkers for Huntington's disease.Journal of neurology · 2023Review
- Identification of biomarkers differentiating Alzheimer's disease from other neurodegenerative diseases by integrated bioinformatic analysis and machine-learning strategies.Frontiers in molecular neuroscience · 2023Article
- TGF-β as a Key Modulator of Astrocyte Reactivity: Disease Relevance and Therapeutic Implications.Biomedicines · 2022Review
- Neuroinflammation in Huntington's Disease: A Starring Role for Astrocyte and Microglia.Current neuropharmacology · 2022Review
- Human iPSC-derived neural precursor cells differentiate into multiple cell types to delay disease progression following transplantation into YAC128 Huntington's disease mouse model.Cell proliferation · 2021Article
- Is TGF-β1 a Biomarker of Huntington's Disease Progression?Journal of clinical medicine · 2021Article
- Improving Cognition with Nutraceuticals Targeting TGF-β1 Signaling.Antioxidants (Basel, Switzerland) · 2021Review
- Astrocytes from cortex and striatum show differential responses to mitochondrial toxin and BDNF: implications for protection of striatal neurons expressing mutant huntingtin.Journal of neuroinflammation · 2020Article
- Reduced Fractalkine Levels Lead to Striatal Synaptic Plasticity Deficits in Huntington's Disease.Frontiers in cellular neuroscience · 2020Article
- Transcriptional regulatory networks underlying gene expression changes in Huntington's disease.Molecular systems biology · 2018Article
- The role of TGF-β superfamily signaling in neurological disorders.Acta biochimica et biophysica Sinica · 2018Review
- SMAD transcription factors are altered in cell models of HD and regulate HTT expression.Cellular signalling · 2017Article
- Altered Expression of Matrix Metalloproteinases and Their Endogenous Inhibitors in a Human Isogenic Stem Cell Model of Huntington's Disease.Frontiers in neuroscience · 2017Article
Corrections and comments
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Authors and funding
16 authors at 7 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A defective expression or activity of neurotrophic factors, such as brain- and glial-derived neurotrophic factors, contributes to neuronal damage in Huntington's disease (HD). Here, we focused on transforming growth factor-β (TGF-β(1) ), a pleiotropic cytokine with an established role in mechanisms of neuroprotection. Asymptomatic HD patients showed a reduction in TGF-β(1) levels in the peripheral blood, which was related to trinucleotide mutation length and glucose hypometabolism in the caudate nucleus. Immunohistochemical analysis in post-mortem brain tissues showed that TGF-β(1) was reduced in cortical neurons of asymptomatic and symptomatic HD patients. Both YAC128 and R6/2 HD mutant mice showed a reduced expression of TGF-β(1) in the cerebral cortex, localized in neurons, but not in astrocytes. We examined the pharmacological regulation of TGF-β(1) formation in asymptomatic R6/2 mice, where blood TGF-β(1) levels were also reduced. In these R6/2 mice, both the mGlu2/3 metabotropic glutamate receptor agonist, LY379268, and riluzole failed to increase TGF-β(1) formation in the cerebral cortex and corpus striatum, suggesting that a defect in the regulation of TGF-β(1) production is associated with HD. Accordingly, reduced TGF-β(1) mRNA and protein levels were found in cultured astrocytes transfected with mutated exon 1 of the human huntingtin gene, and in striatal knock-in cell lines expressing full-length huntingtin with an expanded glutamine repeat. Taken together, our data suggest that serum TGF-β(1) levels are potential biomarkers of HD development during the asymptomatic phase of the disease, and raise the possibility that strategies aimed at rescuing TGF-β(1) levels in the brain may influence the progression of HD.
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