ArticleScientific reports2015
Connexin26 gap junction mediates miRNA intercellular genetic communication in the cochlea and is required for inner ear development.
Article in Scientific reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 56 citations in OpenAlex.
- Recent Progress in Mechanism-Based Therapies forInternational journal of molecular sciences · 2026Review
- Connexin 26 Functions as a Direct Transcriptional Regulator During the Cochlea Development.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Distinct Connexin43, Connexin31, and Pannexin1 expression patterns in the cochlea of a non-human primate.Scientific reports · 2025Article
- MicroRNA Gets a Mighty Award.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Review
- Exosomes and microRNAs as mediators of the exercise.European journal of medical research · 2025Review
- Promotion of Cx26 mutants located in TM4 region for membrane translocation successfully rescued hearing loss.Theranostics · 2025Article
- Modeling of auditory neuropathy spectrum disorders associated with theFrontiers in molecular neuroscience · 2024Article
- Functional Consequences of Pathogenic Variants of theBiomolecules · 2023Review
- Cytomembrane Trafficking Pathways of Connexin 26, 30, and 43.International journal of molecular sciences · 2023Review
- Preservation of developmental spontaneous activity enables early auditory system maturation in deaf mice.PLoS biology · 2023Article
- Cx26 heterozygous mutations cause hyperacusis-like hearing oversensitivity and increase susceptibility to noise.Science advances · 2023Article
- The protective effects of systemic dexamethasone on sensory epithelial damage and hearing loss in targeted Cx26-null mice.Cell death & disease · 2022Article
- Article
- Regeneration in the Auditory Organ in Cuban and African Dwarf Crocodiles (Frontiers in cell and developmental biology · 2022Article
- The role of gap junctions in cell death and neuromodulation in the retina.Neural regeneration research · 2021Review
- Whole exome sequencing, in silico and functional studies confirm the association of theSaudi journal of biological sciences · 2021Article
- RNAs on the Go: Extracellular Transfer in Insects with Promising Prospects for Pest Management.Plants (Basel, Switzerland) · 2021Review
- Congenital Deafness and Recent Advances Towards Restoring Hearing Loss.Current protocols · 2021Article
- F-Actin Dysplasia Involved in Organ of Corti Deformity inFrontiers in molecular neuroscience · 2021Article
- miRNA and mRNA Profiling Links Connexin Deficiency to Deafness via Early Oxidative Damage in the MouseFrontiers in cell and developmental biology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Organ development requires well-established intercellular communication to coordinate cell proliferations and differentiations. MicroRNAs (miRNAs) are small, non-coding RNAs that can broadly regulate gene expression and play a critical role in the organ development. In this study, we found that miRNAs could pass through gap junctions between native cochlear supporting cells to play a role in the cochlear development. Connexin26 (Cx26) and Cx30 are predominant isoforms and co-express in the cochlea. Cx26 deficiency but not Cx30 deficiency can cause cochlear developmental disorders. We found that associated with Cx26 deletion induced the cochlear developmental disorders, deletion of Cx26 but not Cx30 disrupted miRNA intercellular transfer in the cochlea, although inner ear gap junctions still retained permeability after deletion of Cx26. Moreover, we found that deletion of Cx26 but not Cx30 reduced miR-96 expression in the cochlea during postnatal development. The reduction is associated with the cochlear tunnel developmental disorder in Cx26 knockout (KO) mice. These data reveal that Cx26-mediated intercellular communication is required for cochlear development and that deficiency of Cx26 can impair miRNA-mediated intercellular genetic communication in the cochlea, which may lead to cochlear developmental disorders and eventually congenital deafness as previously reported.
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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.