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    Online Resource
    Online Resource
    Oxford University Press (OUP) ; 2018
    In:  Sexual Medicine Vol. 6, No. 4 ( 2018-12-01), p. 339-347
    In: Sexual Medicine, Oxford University Press (OUP), Vol. 6, No. 4 ( 2018-12-01), p. 339-347
    Abstract: Female sexual dysfunction (FSD) is a common disease with serious potential hazards, but it has not received much attention. The pathogenesis of FSD is urgently needed for the diagnosis and treatment of FSD. Aim To investigate the role of microribonucleic acid (mRNA, miR)-137 in FSD. Methods Vaginal epithelium tissues from 15 women with lubrication disorder and 15 women with normal function were collected for this study. The expression level of miR-137 in lubrication disorder and normal function women were measured by microarray analysis and Real-time Quantitative Polymerase Chain Reaction (PCR, qPCR). miR-137 was overexpressed in vaginal epithelial cells VK2/E6E7 by lentivirus infection. The cell water permeability was measured using the calcein-quenching method. Cell apoptosis was analyzed by flow cytometry. The potential target of miR-137 was predicted by bioinformatic analysis, then verified by luciferase reporter assays. Main Outcome Measure The expression level of miR-137 and aquaporin-2 (AQP2), cell water permeability, cell apoptosis, and luciferase reporter assays were examined. Results miR-137 was found to be highly expressed in vaginal epithelial tissues of women with lubrication disorder. Additionally, functional in vitro studies suggested that overexpression of miR-137 leads to a decrease in cell permeability. By combining target prediction and examination, we identified AQP2 as the direct mechanistic target of miR-137 that affected the water permeability of vaginal epithelial cells. Conclusion Our results point to a novel role for miR-137 and its downstream effector AQP2 in vaginal lubrication, which can be manipulated as therapeutic targets against lubrication disorder and its related disorders.
    Type of Medium: Online Resource
    ISSN: 2050-1161
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2018
    detail.hit.zdb_id: 2734882-9
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