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Downregulation of BST2 Rescues Cochlear Nerve Demyelination in Age-Related Hearing Loss via Enhancing Schwann Cell Migration #MMPMID41391004
Liu M; Li Q; Cao H; Yin H; Yang J; Liu T; Wang J; Zhao L; Wang B
Aging Cell 2025[Dec]; ? (?): e70325 PMID41391004show ga
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-kappaB 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-kappaB pathway, thereby enhancing SC migration capacity and promoting MPZ expression.
Aging+Cell 2025 ; ? (?): e70325
