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Characterization of mouse cochlear macrophage enriched and age-dependent gene expression

ABSTRACT: Characterization of mouse cochlear macrophage enriched and age-dependent gene expression

PROVIDER: PRJNA814668 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR18291200.fastq.gz	Fastqsanger.gz
	SRR18291201.fastq.gz	Fastqsanger.gz
	SRR18291173.fastq.gz	Fastqsanger.gz
	SRR18291174.fastq.gz	Fastqsanger.gz
	SRR18291175.fastq.gz	Fastqsanger.gz

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Characterization of mouse cochlear macrophage enriched and age-dependent gene expression

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Project description:Deprivation of peripheral nerve input by cochlear removal in young mice results in dramatic neuron death in the cochlear nucleus (CN). The same manipulation in older mice does not result in significant loss. The molecular basis of this critical period of vulnerability remains largely unknown. Here we identified genes regulated at early time points after cochlear removal at ages when neurons are vulnerable (postnatal day (P)7) or invulnerable (P21) to this challenge. Afferent deprivation regulated very different sets of genes at P7 and P21. These genes showed a variety of functions at both ages, but surprisingly there was no net increase in pro-apoptotic genes at P7. A large set of upregulated immune-related genes was identified at P21. Keywords: Time Course after Cochlear Removal, Age Comparison

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Project description:Outer and inner hair cells in the cochlea are essential for hearing, but are vulnerable to damage by genetic mutations and environmental insults, resulting in irreversible sensorineural hearing loss. Investigating these processes requires access to large numbers of human cochlear hair cells and the ability to precisely control genetic, biochemical, and environmental conditions. We recently established a new organoid system that recapitulates human cochlear differentiation. However, maturation of cochlear organoid cultures is inefficient, requiring several months to express the mature outer hair cell marker Prestin. To efficiently obtain fully functional outer hair cells, we tested the effects of the thyroid hormone thyroxine on hair cell maturation in human cochlear organoids. Thyroxine supplementation significantly increased the percentages of Prestin-positive hair cells in an age-dependent manner. Additionally, transcriptomic analyses revealed upregulation of mature outer hair cell genes and downregulation of immature hair cell genes in thyroxine-treated hair cells. Furthermore, some of the treated hair cells exhibited electromotility, a functional hallmark of mature outer hair cells. These results suggest that thyroid hormones accelerate the maturation of hair cells in human cochlear organoids, thereby useful for establishing an improved in vitro model for pre-clinical investigation on sensorineural hearing loss.

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