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Genomic alterations in Reinke's edema

ABSTRACT: Genomic alterations in Reinke's edema

PROVIDER: PRJNA736237 | ENA |

REPOSITORIES: ENA

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Genomic alterations in Reinke's edema

Project description:Reinke's edema (RE) is a laryngeal lesion related to excessive tobacco smoking, voice overuse, and laryngopharyngeal reflux. Although the risk of malignancy is low, RE has been classified among premalignant lesions. Array-based comparative genomic hybridization (aCGH) was used to investigate DNA copy number alterations (CNA) and as a tool to identify markers of risk stratification.

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Testosterone acts through membrane protein GPRC6A to cause cardiac edema in zebrafish emrbyos

Project description:Classically, intracellular nuclear androgen receptors (ar) are considered to be the key mediators of androgen actions. However, there have been several reports that androgens can also exert their effects by binding to integral membrane proteins. Despite in vitro cloning and characterization of several putative membrane androgen receptors, their functions in vivo remain poorly understood. We used a chemical-genetic screen in zebrafish and discovered that the G-protein coupled receptor, GPRC6A, mediates androgen action during embryonic development. We exposed zebrafish embryos to testosterone (30 μM) from 2-4 hours post-fertilization (hpf) until 72 hpf. We found that testosterone exposure caused cardiac edema in wild-type and ar mutant zebrafish embryos, but there was a significant reduction in this phenotype in the grprc6a mutant embryos, suggesting that gprc6a regulates androgen action independently of nuclear androgen receptors. Additionally, we exposed wild-type embryos to testosterone together with GPRC6A antagonists and observed a significant suppression of the cardiac edema phenotype. These results suggest that testosterone causes cardiac edema in zebrafish embryos by acting via the integral membrane protein GPRC6A, independently of nuclear androgen receptors. Overall, our study provides insights into non-genomic androgen signaling during embryonic development and identifies GPRC6A as a key receptor mediating androgen action.

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