ArticlePloS one2016
miR-196a Ameliorates Cytotoxicity and Cellular Phenotype in Transgenic Huntington's Disease Monkey Neural Cells.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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.
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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.
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Who cites it
24 citing papers in PubMed, 36 citations in OpenAlex.
- The Expanding Role of Non-Coding RNAs in Neurodegenerative Diseases: From Biomarkers to Therapeutic Targets.Pharmaceuticals (Basel, Switzerland) · 2026Review
- Genomic ncRNAs regulating mitochondrial function in neurodegeneration: a neglected clue in the complex etiopathogenesis of multiple sclerosis.Cell & bioscience · 2025Article
- Neuroinflammation and the role of epigenetic-based therapies for Huntington's disease management: the new paradigm.Inflammopharmacology · 2024Review
- The updated development of blood-based biomarkers for Huntington's disease.Journal of neurology · 2023Review
- Non-coding RNAs in human health and disease: potential function as biomarkers and therapeutic targets.Functional & integrative genomics · 2023Review
- miR-196a enhances polymerization of neuronal microfilaments through suppressing IMP3 and upregulating IGF2 in Huntington's disease.Molecular therapy. Nucleic acids · 2022Article
- Epigenetic Changes in Prion and Prion-like Neurodegenerative Diseases: Recent Advances, Potential as Biomarkers, and Future Perspectives.International journal of molecular sciences · 2022Review
- Extracellular Vesicles, Stem Cells and the Role of miRNAs in Neurodegeneration.Current neuropharmacology · 2022Review
- The emerging role of long non-coding RNAs, microRNAs, and an accelerated epigenetic age in Huntington's disease.Frontiers in aging neuroscience · 2022Review
- The regulatory roles of microRNAs toward pathogenesis and treatments in Huntington's disease.Journal of biomedical science · 2021Review
- MicroRNAs in Huntington's Disease: Diagnostic Biomarkers or Therapeutic Agents?Frontiers in cellular neuroscience · 2021Review
- Review
- Functional roles and networks of non-coding RNAs in the pathogenesis of neurodegenerative diseases.Journal of biomedical science · 2020Review
- Circulating RNAs as Potential Biomarkers in Amyotrophic Lateral Sclerosis.International journal of molecular sciences · 2020Review
- Epigenetic mechanisms of neurodegenerative diseases and acute brain injury.Neurochemistry international · 2020Review
- Chromatin accessibility and transcription dynamics during in vitro astrocyte differentiation of Huntington's Disease Monkey pluripotent stem cells.Epigenetics & chromatin · 2019Article
- MicroRNA in Brain pathology: Neurodegeneration the Other Side of the Brain Cancer.Non-coding RNA · 2019Review
- The Emerging Role of microRNAs in Polyglutamine Diseases.Frontiers in molecular neuroscience · 2019Article
- Combination of stem cell and gene therapy ameliorates symptoms in Huntington's disease mice.NPJ Regenerative medicine · 2019Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Huntington's disease (HD) is an inherited neurodegenerative disorder caused by the expansion of polyglutamine (polyQ) tract that leads to motor, cognitive and psychiatric impairment. Currently there is no cure for HD. A transgenic HD nonhuman primate (HD-NHP) model was developed with progressive development of clinical and pathological features similar to human HD, which suggested the potential preclinical application of the HD-NHP model. Elevated expression of miR-196a was observed in both HD-NHP and human HD brains. Cytotoxicity and apoptosis were ameliorated by the overexpression of miR-196a in HD-NHP neural progenitor cells (HD-NPCs) and differentiated neural cells (HD-NCs). The expression of apoptosis related gene was also down regulated. Mitochondrial morphology and activity were improved as indicated by mitotracker staining and the upregulation of CBP and PGC-1α in HD-NPCs overexpressing miR-196a. Here we demonstrated the amelioration of HD cellular phenotypes in HD-NPCs and HD-NCs overexpressing miR-196a. Our results also suggested the regulatory role of miR-196a in HD pathogenesis that may hold the key for understanding molecular regulation in HD and developing novel therapeutics.
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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.