ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Exosomes from MiR-21-5p-Increased Neurons Play a Role in Neuroprotection by Suppressing Rab11a-Mediated Neuronal Autophagy In Vitro After Traumatic Brain Injury.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 63 papers.
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Who cites it
63 citing papers in PubMed, 108 citations in OpenAlex.
- Integrated Necroptosis Within Programmed Cell Death in Traumatic Brain Injury.Molecular neurobiology · 2026Review
- Where and how do mammalian cells shape autophagosomes?The Journal of biological chemistry · 2026Review
- RVG-Modified BMSCs-Derived Small Extracellular Vesicles Loaded With miR-21 Alleviate Neuronal Injury Resulted From Excessive Autophagy via Targeting PTEN/Akt/mTOR Pathway After Cerebral Ischaemia.Journal of extracellular vesicles · 2026Article
- Advances in Intranasal Delivery of Exosomes for Central Nervous System Disorders.Molecular neurobiology · 2025Review
- Mechanisms of Transfer RNA Fragments Functionality Within and Between Cells and Organisms.Cells · 2025Review
- miR-21-5p Alleviates Retinal Ischemia-Reperfusion Injury by Inhibiting M1 Polarization of Microglia via Suppression of STAT3 Signaling.Biomedicines · 2025Article
- Extracellular vesicles as biomarkers for traumatic brain injury using a 3D in vitro human brain tissue model.Scientific reports · 2025Article
- The Application of MicroRNAs in Traumatic Brain Injury: Mechanism Elucidation and Clinical Translation.Molecular neurobiology · 2025Review
- Extracellular Vesicles as Precision Delivery Systems for Biopharmaceuticals: Innovations, Challenges, and Therapeutic Potential.Pharmaceutics · 2025Review
- Mesenchymal stem cell exosomes therapy for the treatment of traumatic brain injury: mechanism, progress, challenges and prospects.Journal of translational medicine · 2025Review
- BMSCs-derived small extracellular vesicles antagonize cerebral endothelial Caveolin-1 driven autophagic degradation of tight-junction proteins to protect blood-brain barrier post-stroke.International journal of biological sciences · 2025Article
- MiR338-3p expression in extracellular vesicles after severe trauma with or without traumatic brain injury.Brain communications · 2025Article
- The role of autophagy in brain health and disease: Insights into exosome and autophagy interactions.Heliyon · 2024Review
- The Ambivalent Role of miRNA-21 in Trauma and Acute Organ Injury.International journal of molecular sciences · 2024Review
- Dynamic Changes and Effects of HBiochemical genetics · 2024Article
- Applications of Stem Cell-Derived Extracellular Vesicles in Nerve Regeneration.International journal of molecular sciences · 2024Review
- Autophagy-modulating biomaterials: multifunctional weapons to promote tissue regeneration.Cell communication and signaling : CCS · 2024Review
- Extracellular Vesicles: Therapeutic Potential in Central Nervous System Trauma by Regulating Cell Death.Molecular neurobiology · 2023Review
- Role of exosomal ncRNAs in traumatic brain injury.Non-coding RNA research · 2023Review
- Rab11a in the spinal cord: an essential contributor to complete Freund's adjuvant-induced inflammatory pain in mice.Molecular brain · 2023Article
3 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND Traumatic brain injury (TBI) produces a series of pathological processes. Recent studies have indicated that autophagy pathway is persistently activated after TBI, which may lead to deterioration of nerve injury. Our preliminary work found miR-21-5p was upregulated in both in vivo and in vitro TBI models. MicroRNAs (miRNAs) could be loaded into exosomes to perform cell-to-cell interactions. This research aimed to evaluate the therapeutic effect of neuron-derived exosomes enriched with miR-21-5p on the TBI in vitro and to further explore the possible mechanisms. MATERIAL AND METHODS Brain extracts harvested from an rTBI mouse model were added to cultured HT-22 neurons to imitate the microenvironment of injured brain on in vitro cultured cells. Ultracentrifugation was performed to isolate exosomes. Transmission electron microscopy and Nano sight technology were used to examine exosomes. An in vitro model of TBI was established to study the effect of exosomal miR-21-5p on nerve injury and on neuronal autophagy regulation. RESULTS The expression of miR-21-5p was increased in exosomes derived from HT-22 neurons after treatment with rTBI mouse brain extracts. Autophagy was activated in HT-22 neurons after scratch injury. Exosomal miR-21-5p produced a protective effect by suppressing autophagy in a TBI model in vitro. MiR-21-5p could directly target the Rab11a 3'UTR region to reduce its translation and further suppressed Rab11a-mediated neuronal autophagy. CONCLUSIONS The levels of miR-21-5p in neuronal exosomes increased from the acute to the chronic phase of TBI. Neuronal exosomes enriched with miR-21-5p can inhibit the activity of neuronal autophagy by targeting Rab11a, thus attenuating trauma-induced, autophagy-mediated nerve injury in vitro.
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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.