ArticleJournal of inorganic biochemistry2013
Expression of the phagocytosis-essential protein TREM2 is down-regulated by an aluminum-induced miRNA-34a in a murine microglial cell line.
Article in Journal of inorganic biochemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 66 citations in OpenAlex.
- Targeting TREM2 for Parkinson's Disease: Where to Go?Frontiers in immunology · 2021Pooled it
- Role of TREM2 in neuroinflammation regulation: mechanisms, disease associations, and therapeutic translation advances.Journal of translational medicine · 2025Review
- Modulatory potential of A novel benzofuran-derived compound against aluminium chloride-induced neurotoxicity and miRNA dysregulation: Biochemical and bio-analytical study.Toxicology reports · 2025Article
- The neuroinflammatory role of microRNAs in Alzheimer's disease: pathological insights to therapeutic potential.Molecular and cellular biochemistry · 2025Review
- Epigenetic Mechanisms of Aluminum-Induced Neurotoxicity and Alzheimer's Disease: A Focus on Non-Coding RNAs.Neurochemical research · 2024Review
- MicroRNAs regulation in Parkinson's disease, and their potential role as diagnostic and therapeutic targets.NPJ Parkinson's disease · 2024Review
- MicroRNAs in microglia: deciphering their role in neurodegenerative diseases.Frontiers in cellular neuroscience · 2024Review
- The effects and potential of microglial polarization and crosstalk with other cells of the central nervous system in the treatment of Alzheimer's disease.Neural regeneration research · 2023Review
- Review
- Microglial Activation in Metal Neurotoxicity: Impact in Neurodegenerative Diseases.BioMed research international · 2023Review
- Alteration of Biomolecular Conformation by Aluminum-Implications for Protein Misfolding Disease.Molecules (Basel, Switzerland) · 2022Article
- New models of Parkinson's like neuroinflammation in human microglia clone 3: Activation profiles induced by INF-γ plus high glucose and mitochondrial inhibitors.Frontiers in cellular neuroscience · 2022Article
- MicroRNAs as Potential Orchestrators of Alzheimer's Disease-Related Pathologies: Insights on Current Status and Future Possibilities.Frontiers in aging neuroscience · 2021Review
- MicroRNAs Play a Role in Parkinson's Disease by Regulating Microglia Function: From Pathogenetic Involvement to Therapeutic Potential.Frontiers in molecular neuroscience · 2021Review
- Adult Neural Stem Cell Regulation by Small Non-coding RNAs: Physiological Significance and Pathological Implications.Frontiers in cellular neuroscience · 2021Article
- Molecular mechanisms of aluminum neurotoxicity: Update on adverse effects and therapeutic strategies.Advances in neurotoxicology · 2021Article
- Epigenetic Modulation of Microglia Function and Phenotypes in Neurodegenerative Diseases.Neural plasticity · 2021Review
- microRNA-Based Biomarkers in Alzheimer's Disease (AD).Frontiers in neuroscience · 2020Review
- The Ambiguous Role of Microglia in Aβ Toxicity: Chances for Therapeutic Intervention.Current neuropharmacology · 2020Review
- Curcumin, Gut Microbiota, and Neuroprotection.Nutrients · 2019Review
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
Abstract
One of the key classical pathological features of Alzheimer's disease (AD) is the progressive accumulation of amyloid beta (Aβ42) peptides and their coalescence into highly insoluble senile plaque cores. A major factor driving Aβ42 peptide accumulation is the inability of brain cells to effectively clear excessive amounts of Aβ42 via phagocytosis. The trans-membrane spanning, sensor-receptor known as the "triggering receptor expressed in myeloid cells 2" (TREM2; chr6p21) is essential in the sensing, recognition, phagocytosis and clearance of noxious cellular debris from brain cells, including neurotoxic Aβ42 peptides. Recently, mutations in the TREM2 gene have been associated with amyloidogenesis in neurodegenerative diseases including AD. In this report, we provide evidence that aluminum-sulfate, when incubated with microglial cells, induces the up-regulation of an NF-кB-sensitive micro RNA-34a (miRNA-34a; chr1p36) that is known to target the TREM2 mRNA 3'-untranslated region (3'-UTR), significantly down-regulating TREM2 expression. The aluminum-induced up-regulation of miRNA-34a and down-regulation of TREM2 expression were effectively quenched using the natural phenolic compound and NF-kB inhibitor CAPE [2-phenylethyl-(2E)-3-(3,4-dihydroxyphenyl) acrylate; caffeic-acid phenethyl ester]. These results suggest, for the first time, that an epigenetic mechanism involving an aluminum-triggered, NF-kB-sensitive, miRNA-34a-mediated down-regulation of TREM2 expression may impair phagocytic responses that ultimately contribute to Aβ42 peptide accumulation, aggregation, amyloidogenesis and inflammatory degeneration in the brain.
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Registered trials
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