What is it about?
We identified candidate miRNAs that can interfere post-transcriptionally with the Sirt1-p53 axis. We show that Sirt1 protein, which is known to mediate age-related hearing loss and vascular aging, is down-regulated in the SV of Cx30-/- mice, which correlates with an increment of p53 and oxidative stress at post-natal day 5. Therefore, we propose a pathogenic mechanism mediated by the Sirt1-p53 axis, which leads to an early inner ear oxidative stress damage in the cochlear SV and culminates in its blood barrier disruption (as documented in adult mice at 3 months of age).
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Why is it important?
To our knowledge, this is the first work investigating the role of gene expression regulation by miRNAs during early cochlear development in a Cx30-/- mouse model of DFNB1. Our findings provide new critical evidence related to RNA disease interaction and the role played by oxidative stress and p53-Sirt1 axis in the pathogenesis of both inherited and age-related hearing loss.
Perspectives
Further studies are needed to explore the identified biomarkers for early therapeutic intervention.
Giulia Gentile
Consiglio Nazionale delle Ricerche
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This page is a summary of: miRNA and mRNA Profiling Links Connexin Deficiency to Deafness via Early Oxidative Damage in the Mouse Stria Vascularis, Frontiers in Cell and Developmental Biology, January 2021, Frontiers,
DOI: 10.3389/fcell.2020.616878.
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