ArticleDisease markers2021
miR-29a-5p Alleviates Traumatic Brain Injury- (TBI-) Induced Permeability Disruption via Regulating NLRP3 Pathway.
Article in Disease markers, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 26 citations in OpenAlex.
- Exercise mimetics: molecular mechanisms, biological and therapeutic effects.Molecular biomedicine · 2026Review
- Interplay Among Endothelial Dysfunction, NLRP3 Pathway Activation, and microRNAs in the Pathogenesis of Preeclampsia.Diseases (Basel, Switzerland) · 2026Review
- MicroRNA-29a-5p contributes to neuroinflammation through TLR7.Journal of neuroinflammation · 2026Article
- Extracellular RNAs as Messengers and Early Biomarkers in Neurodegeneration.International journal of molecular sciences · 2025Review
- Neutrophil extracellular traps aggravate blood-brain barrier disruption via ZBP1/FSP1-mediated ferroptosis after traumatic brain injury.Fluids and barriers of the CNS · 2025Article
- The Application of MicroRNAs in Traumatic Brain Injury: Mechanism Elucidation and Clinical Translation.Molecular neurobiology · 2025Review
- Short-term exposure to particulate matter triggers a selective alteration of plasma extracellular vesicle-packaged miRNAs in a mouse model of multiple sclerosis.Frontiers in immunology · 2025Article
- Article
- NLRP3 Inflammasome Inhibitors for Antiepileptogenic Drug Discovery and Development.International journal of molecular sciences · 2024Review
- New Insights on NLRP3 Inflammasome: Mechanisms of Activation, Inhibition, and Epigenetic Regulation.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2024Review
- Role of regulatory non-coding RNAs in traumatic brain injury.Neurochemistry international · 2024Review
- Potential Regulation of miRNA-29 and miRNA-9 by Estrogens in Neurodegenerative Disorders: An Insightful Perspective.Brain sciences · 2023Review
- Interleukin-35 attenuates blood-brain barrier dysfunction caused by cerebral ischemia-reperfusion injury through inhibiting brain endothelial cell injury.Annals of translational medicine · 2022Article
- Acute Ethanol Challenge Differentially Regulates Expression of Growth Factors and miRNA Expression Profile of Whole Tissue of the Dorsal Hippocampus.Frontiers in neuroscience · 2022Article
- Inhibition of circular RNA circ_0138959 alleviates pyroptosis of human gingival fibroblasts via the microRNA-527/caspase-5 axis.Bioengineered · 2022Article
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveInactivation of NLRP3 inflammasome plays a role in reducing the permeability of endothelial cells and improving blood-brain barrier (BBB) dysfunction following traumatic brain injury (TBI). However, the mechanism controlling NLRP3 inflammasome activation remains unclear. This study is aimed at defining the role of miR-29a-5p in NLRP3 inflammasome activation and permeability of endothelial cells under TBI.
methodsThe scratch injury model on brain bEnd.3 microvascular endothelial cells was used as in vitro TBI model cells. Effects of miR-29a mimics and inhibitors on TBI model cells were observed by examining their action on FITC, TEER, and protein contents of ZO-1 and occludin, and cell permeability-associated protein. Luciferase reporter assay evaluated miR-29a-5p targeting to NLRP3. ELISA examined of IL-1
resultsmiR-29a-3p and miR-29a-5p mimics decrease the concentration of FITC, and increase TEER and the protein contents of ZO-1 and occludin in TBI model cells. miR-29a-5p silencing disrupted the permeability of mouse bEnd.3 cells. miR-29a-5p targets to NLRP3 through the binding on its 3'UTR and negatively regulates its expression in TBI model cells. NLRP3 inhibition and miR-29a-5p silencing together caused significantly decreased FITC concentration and increased TEER value and release of IL-1
conclusionsmiR-29a-5p mimics protect TBI-induced increased endothelial cell permeability and BBB dysfunction via suppressing NLRP3 expression and activation.
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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.