ArticleCell death & disease2014
MicroRNA-23a/b and microRNA-27a/b suppress Apaf-1 protein and alleviate hypoxia-induced neuronal apoptosis.
Article in Cell death & disease, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 107 papers, 2 of them syntheses that pooled it.
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Who cites it
107 citing papers in PubMed, 2 syntheses or guidelines pooled it, 163 citations in OpenAlex.
- Potential Exosome Biomarkers for Parkinson's Disease Diagnosis: A Systematic Review and Meta-Analysis.International journal of molecular sciences · 2024Pooled it
- Systematic Review of the Diagnostic and Clinical Utility of Salivary microRNAs in Traumatic Brain Injury (TBI).International journal of molecular sciences · 2022Pooled it
- Development of hexaplex PCR assay for the detection and characterization common tick-borne pathogens in dogs, and analysis of risk factors.Veterinary and animal science · 2026Article
- RNA biomarkers in spinal muscular atrophy: enhancing pathogenesis understanding and guiding precision medicine.Cellular and molecular life sciences : CMLS · 2026Review
- MicroRNA-mediated regulation of proliferation, lineage differentiation, and apoptosis in neural stem cells.RNA biology · 2025Review
- The multiplex crosstalk between non-coding RNAs, programmed cell death and related mechanisms: a dynamic duo in hematological malignancies.Cancer cell international · 2025Review
- Bio fluid exosomes: promises, challenges, and future directions in translational medicine.Journal of translational medicine · 2025Review
- MiR-27b-3p Reduces the Efficacy of Propranolol in the Treatment of Infantile Hemangioma by Inhibiting the Expression of Apaf-1.Biomedicines · 2025Article
- Human Schwann Cell-Derived Extracellular Vesicle Isolation, Bioactivity Assessment, and Omics Characterization.International journal of nanomedicine · 2025Article
- Exercise-Intervened Endothelial Progenitor Cell Exosomes Protect N2a Cells by Improving Mitochondrial Function.International journal of molecular sciences · 2024Article
- Analysis of Plasma-Derived Exosomal MicroRNAs as Potential Biomarkers for Canine Idiopathic Epilepsy.Animals : an open access journal from MDPI · 2024Article
- Investigating microRNAs as biomarkers in disorders of consciousness: a longitudinal multicenter study.Scientific reports · 2023Article
- MicroRNAs: protective regulators for neuron growth and development.Neural regeneration research · 2023Review
- The potential of targeting microRNA-23b-3p signaling in Alzheimer's disease: opinions on recent findings.Frontiers in pharmacology · 2023Article
- MALAT1 MediatesMediators of inflammation · 2023Article
- ISGylation is induced in neurons by demyelination driving ISG15-dependent microglial activation.Journal of neuroinflammation · 2022Article
- Review
- Response of plasma microRNAs to nusinersen treatment in patients with SMA.Annals of clinical and translational neurology · 2022Article
- miR-23b-3p rescues cognition in Alzheimer's disease by reducing tau phosphorylation and apoptosis via GSK-3β signaling pathways.Molecular therapy. Nucleic acids · 2022Article
- Review
47 more citing papers are in PubMed but not listed here.
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Expression of apoptotic protease activating factor-1 (Apaf-1) gradually decreases during brain development, and this decrease is likely responsible for the decreased sensitivity of brain tissue to apoptosis. However, the mechanism by which Apaf-1 expression is decreased remains elusive. In the present study, we found that four microRNAs (miR-23a/b and miR-27a/b) of miR-23a-27a-24 and miR-23b-27b-24 clusters play key roles in modulating the expression of Apaf-1. First, we found that miR-23a/b and miR-27a/b suppressed the expression of Apaf-1 in vitro. Interestingly, the expression of the miR-23-27-24 clusters in the mouse cortex gradually increased in a manner that was inversely correlated with the pattern of Apaf-1 expression. Second, hypoxic injuries during fetal distress caused reduced expression of the miR-23b and miR-27b that was inversely correlated with an elevation of Apaf-1 expression during neuronal apoptosis. Third, we made neuronal-specific transgenic mice and found that overexpressing the miR-23b and miR-27b in mouse neurons inhibited the neuronal apoptosis induced by intrauterine hypoxia. In conclusion, our results demonstrate, in central neural system, that miR-23a/b and miR-27a/b are endogenous inhibitory factors of Apaf-1 expression and regulate the sensitivity of neurons to apoptosis. Our findings may also have implications for the potential target role of microRNAs in the treatment of neuronal apoptosis-related diseases.
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