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Beta-Catenin signaling is essential for mammalian larynx recanalization and establishment of vocal fold progenitor cells.
Development. 2018 Jan 31;:
Authors: Lungova V, Verheyden JM, Sun X, Thibeault SL
Abstract
Congenital laryngeal webs result from failure of vocal fold separation during development in utero. Infants present with life-threatening respiratory problems at birth; extensive lifelong difficulties in breathing and voicing. The molecular mechanisms that instruct vocal fold formation are rarely studied. Here we show, for the first time, that conditional inactivation of β-Catenin in the primitive laryngopharyngeal epithelium leads to failure in separation of the vocal folds approximating the gross phenotype of laryngeal webbing. These defects can be traced to a series of morphogenesis defects, including delayed fusion of the epithelial lamina and formation of the laryngeal cecum, failed separation of the larynx and esophagus with reduced and disorganized cartilages and muscles. Parallel to these morphogenesis defects, inactivation of β-Catenin disrupts stratification of epithelial cells and establishment of p63+ basal progenitors. These findings provide the first line of evidence linking β-Catenin function to the cell proliferation and progenitor establishment during larynx and vocal fold development.
PMID: 29386246 [PubMed - as supplied by publisher]
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