ArticleHuman molecular genetics2018
MIR137 schizophrenia-associated locus controls synaptic function by regulating synaptogenesis, synapse maturation and synaptic transmission.
Article in Human molecular genetics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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Who cites it
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 75 citations in OpenAlex.
- Epigenetic mechanisms in schizophrenia and other psychotic disorders: a systematic review of empirical human findings.Molecular psychiatry · 2020Pooled it
- Metabolic crosstalk in the ageing brain: astrocyte-neuron coupling as a target for homeostatic restoration and therapy.Translational neurodegeneration · 2026Review
- Biological underpinnings and genetic predisposition to schizophrenia within microrna-137 regulatory pathways across brain development.Translational psychiatry · 2026Article
- MicroRNAs as biomarkers and molecular mediators of cognitive dysfunction in schizophrenia.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- A non-coding RNA risk pathway in schizophrenia: miR-137 enhances the lncRNA GOMAFU through a pathological transcription network.Translational psychiatry · 2025Article
- MicroRNAs and synaptic dysfunction in Parkinson's disease.Molecular therapy. Nucleic acids · 2025Review
- Dysregulation of MiRNAs in schizophrenia in an Egyptian patient population.Scientific reports · 2025Article
- Alteration of microRNA expression in lymphocytes in patients with first-episode schizophrenia.BMC psychiatry · 2025Article
- An increased copy number of glycine decarboxylase (GLDC) associated with psychosis reduces extracellular glycine and impairs NMDA receptor function.Molecular psychiatry · 2025Article
- Decoding the Molecular Mechanisms of miRNAs: Protein Interactions in Schizophrenia Pathogenesis.Current protein & peptide science · 2025Review
- Schizophrenia risk-associated SNPs affect expression of microRNA 137 host gene: a postmortem study.Human molecular genetics · 2024Article
- Small Differences and Big Changes: The Many Variables of MicroRNA Expression and Function in the Brain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Review
- Article
- L-type calcium channels and neuropsychiatric diseases: Insights into genetic risk variant-associated genomic regulation and impact on brain development.Channels (Austin, Tex.) · 2023Review
- MicroRNA137-loaded lipid nanoparticles regulate synaptic proteins in the prefrontal cortex.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Blue Native PAGE-Antibody Shift in Conjunction with Mass Spectrometry to Reveal Protein Subcomplexes: Detection of a Cerebellar α1/α6-Subunits Containing γ-Aminobutyric Acid Type A Receptor Subtype.International journal of molecular sciences · 2023Article
- Schizophrenia plausible protective effect of microRNA-137 is potentially related to estrogen and prolactin in female patients.Frontiers in psychiatry · 2023Article
- Research Progress on Exosomes and MicroRNAs in the Microenvironment of Postoperative Neurocognitive Disorders.Neurochemical research · 2022Review
- MicroRNA binding site variation is enriched in psychiatric disorders.Human mutation · 2022Article
- MeCP2 loss-of-function dysregulates microRNAs regionally and disrupts excitatory/inhibitory synaptic transmission balance.Hippocampus · 2022Article
Corrections and comments
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Authors and funding
16 authors at 3 institutions in 3 countries.
Funding
Abstract
The MIR137 locus is a replicated genetic risk factor for schizophrenia. The risk-associated allele is reported to increase miR-137 expression and miR-137 overexpression alters synaptic transmission in mouse hippocampus. We investigated the cellular mechanisms underlying these observed effects in mouse hippocampal neurons in culture. First, we correlated the risk allele to expression of the genes in the MIR137 locus in human postmortem brain. Some evidence for increased MIR137HG expression was observed, especially in hippocampus of the disease-associated genotype. Second, in mouse hippocampal neurons, we confirmed previously observed changes in synaptic transmission upon miR-137 overexpression. Evoked synaptic transmission and spontaneous release were 50% reduced. We identified defects in release probability as the underlying cause. In contrast to previous observations, no evidence was obtained for selective synaptic vesicle docking defects. Instead, ultrastructural morphometry revealed multiple effects of miR-137 overexpression on docking, active zone length and total vesicle number. Moreover, proteomic analyses of neuronal protein showed that expression of Syt1 and Cplx1, previously reported as downregulated upon miR-137 overexpression, was unaltered. Immunocytochemistry of synapses overexpressing miR-137 showed normal Synaptotagmin1 and Complexin1 protein levels. Instead, our proteomic analyses revealed altered expression of genes involved in synaptogenesis. Concomitantly, synaptogenesis assays revealed 31% reduction in synapse formation. Taken together, these data show that miR-137 regulates synaptic function by regulating synaptogenesis, synaptic ultrastructure and synapse function. These effects are plausible contributors to the increased schizophrenia risk associated with miR-137 overexpression.
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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.