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Cadherin-26 (CDH26) regulates airway epithelial cell cytoskeletal structure and polarity

机译：Cadherin-26（CDH26）调节气道上皮细胞的细胞骨架结构和极性

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Polarization of the airway epithelial cells (AECs) in the airway lumen is critical to the proper function of the mucociliary escalator and maintenance of lung health, but the cellular requirements for polarization of AECs are poorly understood. Using human AECs and cell lines, we demonstrate that cadherin-26 (CDH26) is abundantly expressed in differentiated AECs, localizes to the cell apices near ciliary membranes, and has functional cadherin domains with homotypic binding. We find a unique and non-redundant role for CDH26, previously uncharacterized in AECs, in regulation of cell–cell contact and cell integrity through maintaining cytoskeletal structures. Overexpression of CDH26 in cells with a fibroblastoid phenotype increases contact inhibition and promotes monolayer formation and cortical actin structures. CDH26 expression is also important for localization of planar cell polarity proteins. Knockdown of CDH26 in AECs results in loss of cortical actin and disruption of CRB3 and other proteins associated with apical polarity. Together, our findings uncover previously unrecognized functions for CDH26 in the maintenance of actin cytoskeleton and apicobasal polarity of AECs.
机译：气道内腔中的气道上皮细胞（AEC）的极化对于粘膜纤毛自动扶梯的正常功能和肺部健康的维持至关重要，但是对AEC极化的细胞要求知之甚少。使用人类AEC和细胞系，我们证明钙黏着蛋白26（CDH26）在分化的AEC中大量表达，位于睫状膜附近的细胞顶点，并具有同型结合的功能性钙黏着蛋白结构域。我们发现CDH26在维持细胞骨架结构中调节细胞间接触和细胞完整性方面具有独特和非冗余的作用，而以前在AEC中尚无此特征。具有成纤维细胞表型的细胞中CDH26的过表达增加了接触抑制并促进了单层形成和皮质肌动蛋白结构。 CDH26表达对于平面细胞极性蛋白的定位也很重要。敲除AEC中的CDH26会导致皮质肌动蛋白损失，并破坏CRB3和其他与顶端极性相关的蛋白质。在一起，我们的发现揭示了CDH26在维持肌动蛋白细胞骨架和AEC的apapobasal极性方面以前未被认识的功能。

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