ArticleInternational journal of clinical and experimental pathology2018
MicroRNA-21 and microRNA-146a negatively regulate the secondary inflammatory response of microglia after intracerebral hemorrhage.
Article in International journal of clinical and experimental pathology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 1 of them a synthesis that pooled it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 19 citations in OpenAlex.
- A Systematic Review of MicroRNAs in Hemorrhagic Neurovascular Disease: Cerebral Cavernous Malformations as a Paradigm.International journal of molecular sciences · 2025Pooled it
- Therapeutic Effects of miR-21-5p-Enriched Milk Extracellular Vesicles on Alzheimer's Disease-Associated Neurotoxicity in Vitro.Cell biochemistry and biophysics · 2026Article
- Middle meningeal artery embolization in chronic subdural hematoma: bridging surgical innovations and molecular mechanisms.Frontiers in surgery · 2026Review
- A novel paradigm for chronic subdural hematoma: regenerative medicine strategies targeting the pathological microenvironment.Frontiers in cell and developmental biology · 2026Review
- Transplanting neural stem cells overexpressing miRNA-21 can promote neural recovery after cerebral hemorrhage through the SOX2/LIN28-let-7 signaling pathway.Animal models and experimental medicine · 2025Article
- Alterations of mRNAs and Non-coding RNAs Associated with Neuroinflammation in Alzheimer's Disease.Molecular neurobiology · 2024Review
- Two-Month Voluntary Ethanol Consumption Promotes Mild Neuroinflammation in the Cerebellum but Not in the Prefrontal Cortex, Hippocampus, or Striatum of Mice.International journal of molecular sciences · 2024Article
- Review
- Mesenchymal stem cell-derived extracellular vesicles protect retina in a mouse model of retinitis pigmentosa by anti-inflammation through miR-146a-Nr4a3 axis.Stem cell research & therapy · 2022Article
- Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets.Frontiers in immunology · 2022Review
- MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy.Frontiers in immunology · 2022Review
- Dysregulation of microRNA and Intracerebral Hemorrhage: Roles in Neuroinflammation.International journal of molecular sciences · 2021Review
- Microglia Susceptibility to Free Bilirubin Is Age-Dependent.Frontiers in pharmacology · 2020Article
- Morin Protects Human Respiratory Cells from PMInternational journal of environmental research and public health · 2019Article
- Phenotypic Effects of Wild-Type and Mutant SOD1 Expression in N9 Murine Microglia at Steady State, Inflammatory and Immunomodulatory Conditions.Frontiers in cellular neuroscience · 2019Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundA secondary inflammatory response is the most important mechanism of injury after intracerebral hemorrhage (ICH). Previous studies found microRNAs (miRs) expressed abnormally in the perihematomal tissue and blood of patients with ICH and demonstrated that miRs were related to pathophysiological changes and prognosis after ICH, and the development of inflammation.
methodsWe induced a microglial inflammatory response by lipopolysaccharide (LPS) to construct a microglial inflammatory model. MiR-21/miR-146a overexpression adenovirus was used to infect microglia to increase miR-21/miR-146a expression. MiR-21, miR-146a, IRAK1, MMP-9, TNF-α, TIMP3 and other inflammatory factors were analyzed. Then, miR-21/miR-146a overexpression adenovirus was injected into rats with ICH to modulate the expression. Inflammation, brain edema, and neurological scores were assessed.
resultsFor in vitro and vivo experiments, overexpression of miR-21/miR-146a decreased the expression of IL-1β, IL-6, IL-8, IRAK1, MMP-9 and TNF-α, meanwhile increased the expression of TIMP3 significantly (P<0.001), compared with the negative control group. Additionally, miR-21 and miR-146a reduced brain edema and improved the neurological function in ICH rats.
conclusionOur study proved that miR-21 and miR-146a could negatively regulate the inflammatory response of microglia after ICH and provided a new theoretical basis for the treatment of secondary inflammatory injury after ICH in humans.
Indexed as
Identifiers
31949711PMC6962877W3008549118What OpenQuestion holds
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.