Downregulation of BST2 Rescues Cochlear Nerve Demyelination in Age-Related Hearing Loss via Enhancing Schwann Cell Migration.
Abstract
Cochlear nerve demyelination is a significant pathogenic factor of age-related hearing loss (ARHL), and Schwann cell (SC) migration function plays a key role in the maintenance and regeneration of myelin sheaths. Here, we found that bone marrow stromal antigen 2 (BST2) is significantly upregulated in cochlear SCs during aging following demyelination and hearing loss. However, specific knockdown of BST2 in SCs could obviously improve the SCs migration and the myelin sheath structure manifested in a reduction of E-cadherin expression and increased N-cadherin expression. Further mechanism analysis revealed that POU class 6 homeobox 1 (POU6F1) expression via the NF-κB pathwayleads to enhanced SCs migration ability and increased expression of the myelin protein zero (MPZ), thereby alleviating nerve demyelination and rescuing hearing loss. This study identifies BST2 as a novel therapeutic target for ARHL intervention. In conclusion, the specific downregulation of BST2 in cochlear SCs rescues age-related demyelination and hearing loss by activating the POU6F1/NF-κB pathway, thereby enhancing SC migration capacity and promoting MPZ expression.
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Research summary
The paper claims that downregulation of BST2 in cochlear Schwann cells enhances their migration and alleviates age-related demyelination and hearing loss. This research addresses a specific mechanism related to age-related hearing loss, which is a consequence of aging, thus contributing to understanding and potentially mitigating aspects of age-related decline.
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