ArticleThe Journal of international medical research2020
MiR-26a inhibits the inflammatory response of microglia by targeting HMGA2 in intracerebral hemorrhage.
Article in The Journal of international medical research, 2020. 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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The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
15 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 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
- Nrf2 attenuates neuroinflammatory injury in intracerebral hemorrhage via an ASK1/JNK-related signaling pathway.Scientific reports · 2026Article
- The neurobiological regulatory mechanism of brain edema.Frontiers in cellular neuroscience · 2026Review
- Parkinson's Disease and MicroRNAs: A Duel Between Inhibition and Stimulation of Apoptosis in Neuronal Cells.Molecular neurobiology · 2024Review
- Mesoporous Core-Cone Silica Nanoparticles Can Deliver miRNA-26a to Macrophages to Exert Immunomodulatory Effects on Osteogenesis In Vitro.Nanomaterials (Basel, Switzerland) · 2023Article
- TUG1 aggravates intracerebral hemorrhage injury by inhibiting angiogenesis in an miR-26a-dependent manner.American journal of translational research · 2023Article
- ISGylation is induced in neurons by demyelination driving ISG15-dependent microglial activation.Journal of neuroinflammation · 2022Article
- High-frequency repetitive transcranial magnetic stimulation (rTMS) protects against ischemic stroke by inhibiting M1 microglia polarization through let-7b-5p/HMGA2/NF-κB signaling pathway.BMC neuroscience · 2022Article
- Small interfering RNAs based therapies for intracerebral hemorrhage: challenges and progress in drug delivery systems.Neural regeneration research · 2022Review
- MiR-26a Reduces Inflammatory Responses via Inhibition of PGE2 Production by Targeting COX-2.Inflammation · 2022Article
- Circulating miRNA Correlates with Lipid Profile and Disease Activity in Psoriatic Arthritis, Rheumatoid Arthritis, and Ankylosing Spondylitis Patients.Biomedicines · 2022Article
- MicroRNAs modulate neuroinflammation after intracerebral hemorrhage: Prospects for new therapy.Frontiers in immunology · 2022Review
- HMGA2 Promotes Brain Injury in Rats with Cerebral Infarction by Activating TLR4/NF-Mediators of inflammation · 2022Article
- Clock Gene Nr1d1 Alleviates Retinal Inflammation Through Repression of Hmga2 in Microglia.Journal of inflammation research · 2021Article
- Behavioral Assessment of Sensory, Motor, Emotion, and Cognition in Rodent Models of Intracerebral Hemorrhage.Frontiers in neurology · 2021Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveIntracerebral hemorrhage (ICH) is a common cerebrovascular disease with high mortality and poor prognosis. Therefore, the biological function and underlying molecular mechanism of miR-26a in inflammatory injury following ICH was investigated.
methodsThe potential role of miR-26a was investigated in lipopolysaccharide (LPS)-treated microglial cells by quantitative real-time PCR. To explore the potential role of HMGA2 in the miR-26a-regulated inflammatory response, LPS-induced microglial cells were cotransfected with an miR-26a mimic and pcDNA-HMGA2. Then, lentivirus-mediated overexpression of an miR-26a mimic in mouse microglial cells was performed, and the effects of miR-26a treatment on IL-6, IL-1β, and TNF-α expression in the mouse brain, neurological behavior, and rotarod test performance of mice after ICH were observed.
resultsMiR-26a was significantly downregulated in LPS-treated microglia and ICH mouse models. MiR-26a markedly reduced IL-6, IL-1β, and TNF-α expression in LPS-treated microglial cells. Furthermore, HMGA2 was verified as a direct target of miR-26a. In vivo, miR-26a overexpression in mouse microglial cells significantly suppressed proinflammatory cytokine expression in mouse brains and markedly improved the neurological behavior and rotarod test performance of mice after ICH.
conclusionMiR-26a remarkably inhibited proinflammatory cytokine release by targeting HMGA2, indicating that miR-26a could protect against secondary brain injury following ICH.
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Registered trials
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