ArticleFrontiers in immunology2022
Extracellular Vesicles From Hyperammonemic Rats Induce Neuroinflammation in Cerebellum of Normal Rats: Role of Increased TNFα Content.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 27 citations in OpenAlex.
- Extracellular vesicles from plasma of patients with minimal hepatic encephalopathy induce neuroinflammation and cognitive impairment in rats, which are prevented by treating the patients with rifaximin.Journal of neuroinflammation · 2026Article
- Liver-nervous system axis: pathways, dysregulation, and translational perspectives.Journal of neuroinflammation · 2026Review
- The Role of GABA Pathway Components in Pathogenesis of Neurodevelopmental Disorders.International journal of molecular sciences · 2025Review
- Elevated Plasma BDNF in Early Primary Biliary Cholangitis: Associations with Liver Fibrosis, IL-6, IL-18, Fatigue, and Cognitive Impairment.International journal of molecular sciences · 2025Observational
- Extracellular Vesicles from Peripheral Blood Mononuclear Cells of Hyperammonemic Rats Induce Neuroinflammation in Hippocampus, Impairing Memory and Learning in Normal Rats.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Extracellular vesicle-mediated bidirectional communication between the liver and other organs: mechanistic exploration and prospects for clinical applications.Journal of nanobiotechnology · 2025Review
- Ammonia and beyond - biomarkers of hepatic encephalopathy.Metabolic brain disease · 2025Review
- Motor performance as a predictor of blood levels of ammonia and inflammatory biomarkers in patients with liver cirrhosis.PloS one · 2025Article
- Hyperammonemia increases the release of pathological extracellular vesicles from monocytes by impairing lysosomal function and autophagy through the TNFα-cAMP-PKA-LC3 pathway.Frontiers in immunology · 2025Article
- The Role of Neuroinflammation in the Pathogenesis of Hepatic Encephalopathy.Journal of immunology research · 2025Review
- Role of Redox Homeostasis in the Communication Between Brain and Liver Through Extracellular Vesicles.Antioxidants (Basel, Switzerland) · 2024Review
- Role of peripheral inflammation in minimal hepatic encephalopathy.Metabolic brain disease · 2024Review
- Preface for the Vicente Felipo Honorary Issue of Neurochemical Research.Neurochemical research · 2024Article
- Contribution of extracellular vesicles to neuroinflammation and cognitive and motor deficits in hyperammonemia and hepatic encephalopathy.Extracellular vesicles and circulating nucleic acids · 2024Review
- BDNF and Cerebellar Ataxia.Current drug research reviews · 2024Review
- Pathological and therapeutic effects of extracellular vesicles in neurological and neurodegenerative diseases.Neural regeneration research · 2024Review
- Bidirectional Communication Between the Brain and Other Organs: The Role of Extracellular Vesicles.Cellular and molecular neurobiology · 2023Review
- Extracellular vesicles from hyperammonemic rats induce neuroinflammation in hippocampus and impair cognition in control rats.Cellular and molecular life sciences : CMLS · 2023Article
- Cellular Pathogenesis of Hepatic Encephalopathy: An Update.Biomolecules · 2023Review
- Extracellular vesicles from mesenchymal stem cells reduce neuroinflammation in hippocampus and restore cognitive function in hyperammonemic rats.Journal of neuroinflammation · 2023Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Hyperammonemia plays a main role in the neurological impairment in cirrhotic patients with hepatic encephalopathy. Rats with chronic hyperammonemia reproduce the motor incoordination of patients with minimal hepatic encephalopathy, which is due to enhanced GABAergic neurotransmission in cerebellum as a consequence of neuroinflammation. Extracellular vesicles (EVs) could play a key role in the transmission of peripheral alterations to the brain to induce neuroinflammation and neurological impairment in hyperammonemia and hepatic encephalopathy. EVs from plasma of hyperammonemic rats (HA-EVs) injected to normal rats induce neuroinflammation and motor incoordination, but the underlying mechanisms remain unclear. The aim of this work was to advance in the understanding of these mechanisms. To do this we used an ex vivo system. Cerebellar slices from normal rats were treated ex vivo with HA-EVs. The aims were: 1) assess if HA-EVs induce microglia and astrocytes activation and neuroinflammation in cerebellar slices of normal rats, 2) assess if this is associated with activation of the TNFR1-NF-kB-glutaminase-GAT3 pathway, 3) assess if the TNFR1-CCL2-BDNF-TrkB pathway is activated by HA-EVs and 4) assess if the increased TNFα levels in HA-EVs are responsible for the above effects and if they are prevented by blocking the action of TNFα. Our results show that ex vivo treatment of cerebellar slices from control rats with extracellular vesicles from hyperammonemic rats induce glial activation, neuroinflammation and enhance GABAergic neurotransmission, reproducing the effects induced by hyperammonemia
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