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首页> 外文期刊>Molecular biology of the cell >Desmocollin-2 promotes intestinal mucosal repair by controlling integrin-dependent cell adhesion and migration
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Desmocollin-2 promotes intestinal mucosal repair by controlling integrin-dependent cell adhesion and migration

机译：Desmocollin-2通过控制整联蛋白依赖性细胞粘附和迁移来促进肠粘膜修复

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摘要

The intestinal mucosa is lined by a single layer of epithelial cells that forms a tight barrier, separating luminal antigens and microbes from underlying tissue compartments. Mucosal damage results in a compromised epithelial barrier that can lead to excessive immune responses as observed in inflammatory bowel disease. Efficient wound repair is critical to reestablish the mucosal barrier and homeostasis. Intestinal epithelial cells (IEC) exclusively express the desmosomal cadherins, Desmoglein-2 and Desmocollin-2 (Dsc2) that contribute to mucosal homeostasis by strengthening intercellular adhesion between cells. Despite this important property, specific contributions of desmosomal cadherins to intestinal mucosal repair after injury remain poorly investigated in vivo. Here we show that mice with inducible conditional knockdown (KD) of Dsc2 in IEC (Villin-Cre(ERT2); Dsc2(fl/fl)) exhibited impaired mucosal repair after biopsy-induced colonic wounding and recovery from dextran sulfate sodium-induced colitis. In vitro analyses using human intestinal cell lines after KD of Dsc2 revealed delayed epithelial cell migration and repair after scratch-wound healing assay that was associated with reduced cell-matrix traction forces, decreased levels of integrin beta 1 and beta 4, and altered activity of the small GTPase Rap1. Taken together, these results demonstrate that epithelial Dsc2 is a key contributor to intestinal mucosal wound healing in vivo.
机译：肠粘膜由一层上皮细胞排列，其形成紧密的屏障，将腔抗原和微生物分离在底层的组织隔室。粘膜损伤导致损害的上皮屏障，可导致炎性肠病中观察到过量的免疫应答。高效的伤口修复对于重新建立粘膜屏障和稳态至关重要。肠上皮细胞（IEC）专门表达去染色体钙蛋白，DESMOGELIN-2和DESMOCOLIN-2（DSC2），其通过强化细胞间的细胞间粘附而导致粘膜稳态。尽管这种重要的财产，但损伤后去染色体钙粘蛋白对肠粘膜修复的具体贡献仍然在体内仍然很差。在这里，我们显示IEC中DSC2的诱导条件敲低（KD）的小鼠（Villin-Cre2）; DSC2（FL / FL））在活组织检查诱导的结肠伤害和从葡聚糖硫酸钠诱导的结肠炎中恢复后，粘膜修复受损。在体外分析使用人肠道细胞系在DSC2的KD揭示延迟上皮细胞迁移和修复后，刮伤伤口愈合测定与细胞 - 基质牵引力相关的刮擦愈合测定，降低整合蛋白β1和β4的水平，以及改变的活性小GTP酶RAP1。总之，这些结果表明上皮DSC2是体内肠粘膜伤口愈合的关键因素。

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