ArticleOpen medicine (Warsaw, Poland)2023
UHRF1-induced connexin26 methylation is involved in hearing damage triggered by intermittent hypoxia in neonatal rats.
Article in Open medicine (Warsaw, Poland), 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 4 citations in OpenAlex.
- Obstructive sleep apnea and functional hearing loss over 8 years: results from the National Health and Aging Trends Study.American journal of epidemiology · 2026Article
- Comprehensive analysis of aberrant alternative splicing and RNA binding proteins associated with age-related sensorineural hearing loss.Scientific reports · 2025Article
- Epigenetic Modifications in Sensorineural Hearing Loss: Protective Mechanisms and Therapeutic Potential.Current medical science · 2025Review
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4 authors at 2 institutions in 1 country.
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Abstract
Ubiquitin-like with plant homeodomain and ring finger domains 1 (UHRF1) promotes the maintenance of established patterns of DNA methylation in mammalian cells. Extensive methylation of connexin26 (COX26) during hearing impairment has been demonstrated. The present study aims to determine whether UHRF1 can induce the methylation of COX26 in cochlea damaged by intermittent hypoxia (IH). After the establishment of the cochlear injury model through IH treatment or isolation of the cochlea containing Corti's organ, pathological changes were observed via HE staining. Expressions of COX26 and UHRF1 were detected by quantitative reverse-transcription polymerase chain reaction and Western blot. The effect of COX26 methylation levels was analyzed by methylation-specific PCR (MSP). Phalloidin/immunofluorescence staining was used to observe structural changes. The binding relationship between UHRF1 and COX26 was verified by chromatin immunoprecipitation. IH caused cochlear damage, accompanied by increased methylation of COX26 and expression of UHRF1 in the cochlea of neonatal rats. CoCl
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