ArticleOncotarget2017
MicroRNA-27b inhibition promotes Nrf2/ARE pathway activation and alleviates intracerebral hemorrhage-induced brain injury.
Article in Oncotarget, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 47 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
- Changes in the microRNA cargo of granulosa cell-derived extracellular vesicles under oxidative stress in a bovine model.Biological research · 2026Article
- From bench to bedside: nanomedicine development for intracerebral hemorrhage - exploring microenvironment, innovation, and translation.Journal of nanobiotechnology · 2025Review
- Potential Correlation Between Molecular Biomarkers and Oxidative Stress in Traumatic Brain Injury.International journal of molecular sciences · 2025Review
- MiRNAs as potential therapeutic targets and biomarkers for non-traumatic intracerebral hemorrhage.Biomarker research · 2024Review
- Advances in Understanding the Role of NRF2 in Liver Pathophysiology and Its Relationship with Hepatic-Specific Cyclooxygenase-2 Expression.Antioxidants (Basel, Switzerland) · 2023Review
- MicroRNA-27b Impairs Nrf2-Mediated Angiogenesis in the Progression of Diabetic Foot Ulcer.Journal of clinical medicine · 2023Article
- The Transcription Factor NRF2 Has Epigenetic Regulatory Functions Modulating HDACs, DNMTs, and miRNA Biogenesis.Antioxidants (Basel, Switzerland) · 2023Article
- Redox sensitive miR-27a/b/Nrf2 signaling in Cr(VI)-induced carcinogenesis.The Science of the total environment · 2022Article
- Regulation of nuclear factor erythroid-2-related factor 2 as a potential therapeutic target in intracerebral hemorrhage.Frontiers in molecular neuroscience · 2022Review
- Transcript Expression Profiles and MicroRNA Regulation Indicate an Upregulation of Processes Linked to Oxidative Stress, DNA Repair, Cell Death, and Inflammation in Type 1 Diabetes Mellitus Patients.Journal of diabetes research · 2022Article
- Oxidative Stress Following Intracerebral Hemorrhage: From Molecular Mechanisms to Therapeutic Targets.Frontiers in immunology · 2022Review
- Acupuncture Ameliorates Neuronal Cell Death, Inflammation, and Ferroptosis and Downregulated miR-23a-3p After Intracerebral Hemorrhage in Rats.Journal of molecular neuroscience : MN · 2021Article
- miR-181a Mediates Inflammatory Gene Expression After Intracerebral Hemorrhage: An Integrated Analysis of miRNA-seq and mRNA-seq in a Swine ICH Model.Journal of molecular neuroscience : MN · 2021Article
- New epigenetic players in stroke pathogenesis: From non-coding RNAs to exosomal non-coding RNAs.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2021Review
- Potential therapeutic effects of Nrf2 activators on intracranial hemorrhage.Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism · 2021Review
- Fumonisin BArchives of toxicology · 2021Article
- Adaptive and Biological Responses of Buffalo Granulosa Cells Exposed to Heat Stress under In Vitro Condition.Animals : an open access journal from MDPI · 2021Article
- An Update on Antioxidative Stress Therapy Research for Early Brain Injury After Subarachnoid Hemorrhage.Frontiers in aging neuroscience · 2021Review
- MiR-367 alleviates inflammatory injury of microglia by promoting M2 polarization via targeting CEBPA.In vitro cellular & developmental biology. Animal · 2020Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress and neuroinflammation are the key factors leading to secondary brain injury after intracerebral hemorrhage (ICH). We investigated the effects of miR-27b, an oxidative stress-responsive microRNA, on ICH-induced brain injury in rats. The ICH model was induced by intracerebral injection of collagenase. Following ICH, miR-27b expression in the striatum was reduced, whereas expression of Nrf2 mRNA and protein was increased. In PC12 cells, overexpression of miR-27b reduced expression of Nrf2, Hmox1, Sod1 and Nqo1, while miR-27b inhibition had the opposite effects. Dual luciferase reporter assays showed that Nrf2 mRNA was a direct target of miR-27b. Intracerebroventricular injection of miR-27b antagomir and transfection of miR-27b inhibitor inhibited endogenous miR-27b in rats and PC12 cells, respectively. MiR-27b antagomir promoted activation of the ICH-induced Nrf2/ARE pathway and reduced the lipid peroxidation, neuroinflammation, cell death and neurological deficits otherwise seen after ICH. In PC12 cells, the miR-27b inhibitor diminished iron-induced oxidative stress, inflammation and apoptosis, and those effects were blocked by Nrf2 knockdown. These results demonstrate that miR-27b inhibition alleviates ICH-induced brain injury, which may be explained in part by its regulation on the Nrf2/ARE pathway.
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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.