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Publication : Sox2 overexpression alleviates noise-induced hearing loss by inhibiting inflammation-related hair cell apoptosis.

First Author  Chen D Year  2022
Journal  J Neuroinflammation Volume  19
Issue  1 Pages  59
PubMed ID  35227273 Mgi Jnum  J:329144
Mgi Id  MGI:6889987 Doi  10.1186/s12974-022-02414-0
Citation  Chen D, et al. (2022) Sox2 overexpression alleviates noise-induced hearing loss by inhibiting inflammation-related hair cell apoptosis. J Neuroinflammation 19(1):59
abstractText  BACKGROUND: The transcription factor Sox2 plays important roles in the developmental processes of multiple organs and tissues. However, whether Sox2 can protect mature or terminally differentiated cells against injury is still unknown. METHODS: We investigated the roles of Sox2 in cochlear hair cells, which are terminally differentiated cells, using conditional transgenic mice and several hearing loss models. RESULTS: Sox2 overexpression dramatically mitigated the degree of cochlear hair cell loss when exposed to ototoxic drugs. Noise-induced apoptosis of cochlear hair cells and hearing loss were also significantly alleviated by Sox2 overexpression. Notably, noise-induced upregulation of pro-inflammatory factors such as TNF-alpha and IL6 was inhibited by Sox2 overexpression. Then we used lipopolysaccharide to clarify the effect of Sox2 on cochlear inflammation, and Sox2 overexpression significantly inhibited lipopolysaccharide-induced upregulation of pro-inflammatory factors and alleviated inflammation-related cochlear hair cell death. CONCLUSIONS: These results demonstrate a novel protective role of Sox2 in mature and terminally differentiated cochlear hair cells by inhibiting inflammation.
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