Airway epithelial wound repair: role of carbohydrate sialyl Lewis
Airway epithelial wound repair: role of carbohydrate sialyl Lewis
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DOI：
10.1152/ajplung.00120.2006
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发表时间：
2006-10-01
影响因子：
4.9
通讯作者：
Dorscheid, Delbert R.
中科院分区：
文献类型：
--
作者：
Allahverdian, Sima;Wojcik, Kimberly R.;Dorscheid, Delbert R.
气道上皮损伤修复：碳水化合物唾液酸化Lewisx的作用。美国生理学杂志肺细胞分子生理学291：L 828-L 836，2006年。首次发表于2006年6月2日; doi：10.1152/ajplung.00120.2006。上皮修复是一个复杂的细胞和分子过程，其细节仍然不清楚。质膜糖复合物可以通过改变蛋白质和脂质的功能来调节细胞功能。唾液酸化刘易斯（x）（sLe（x））是一种含岩藻糖的四糖，修饰膜结合和分泌蛋白，并介导细胞-细胞相互作用。在本研究中，我们研究了sLe（x）在气道上皮修复中的作用。使用免疫组化，我们发现sLe（x）的表达增加，在受损的支气管上皮与完整的区域相比。机械损伤气道上皮细胞的汇合单层并使其闭合。对受伤的单层进行伤口闭合动力学拍照，固定用于免疫细胞化学研究，或进行RNA提取。检查不同的α 1，3-岩藻糖基转移酶（FucT）的表达，这些酶介导sLe（x）合成的最后一步，我们发现FucT-IV是所有细胞系和原代气道上皮细胞中表达的共同基因。我们证明了机械损伤后sLe（x）的表达随时间增加。用抑制性抗体阻断sLe（x）完全阻止了上皮修复。我们的数据表明sLe（x）在上皮修复中具有重要的功能作用。sLe（x）介导支气管上皮细胞间相互作用促进上皮细胞迁移和修复的确切机制有待进一步研究。
Airway epithelial wound repair: role of carbohydrate sialyl Lewisx. Am J Physiol Lung Cell Mol Physiol 291: L828-L836, 2006. First published June 2, 2006; doi:10.1152/ajplung.00120.2006. Epithelial repair is a complex cellular and molecular process, the details of which are still not clearly understood. Plasma membrane glycoconjugates can modulate cell function by altering the function of protein and lipids. Sialyl Lewis(x) (sLe(x)), a fucose-containing tetrasaccharide, decorates membrane-bound and secreted proteins and mediates cell-cell interaction. In the present study we investigated the role of sLe(x) in airway epithelial repair. Using immunohistochemistry, we showed an increased expression of sLe(x) in areas of damaged bronchial epithelium compared with intact regions. Confluent monolayers of airway epithelial cells were mechanically wounded and allowed to close. Wounded monolayers were photographed for wound closure kinetics, fixed for immunocytochemical studies, or subjected to RNA extraction. Examining the expression of different alpha 1,3-fucosyltransferases (FucT), enzymes that mediate the final step in the synthesis of sLe(x), we found that FucT-IV was the common gene expressed in all cell lines and primary airway epithelial cells. We demonstrated an increased expression of sLe(x) over time after mechanical injury. Blocking of sLe(x) with an inhibitory antibody completely prevented epithelial repair. Our data suggest an essential functional role for sLe(x) in epithelial repair. Further studies are necessary to explore the exact mechanism for sLe(x) in mediating cell-cell interaction in bronchial epithelial cells to facilitate epithelial migration and repair.