伤口愈合
炎症性肠病
细胞生物学
细胞骨架
微管
紧密连接
细胞迁移
结肠炎
溃疡性结肠炎
肌动蛋白
肠上皮
细胞
生物
肠粘膜
肌动蛋白细胞骨架
炎症
上皮
免疫学
医学
病理
疾病
遗传学
内科学
作者
Yanlei Ma,Jiping Yue,Yao Zhang,Chenzhang Shi,Matthew A. Odenwald,Wenguang G. Liang,Qing Wei,Ajay Goel,Xuewen Gou,Jamie V. Zhang,Shao-Yu Chen,Wei-Jen Tang,Jerrold R. Turner,Feng Yang,Hong Liang,Huanlong Qin,Xiaoyang Wu
摘要
Abstract In the intestinal epithelium, the aberrant regulation of cell/cell junctions leads to intestinal barrier defects, which may promote the onset and enhance the severity of inflammatory bowel disease (IBD). However, it remains unclear how the coordinated behaviour of cytoskeletal network may contribute to cell junctional dynamics. In this report, we identified ACF7, a crosslinker of microtubules and F-actin, as an essential player in this process. Loss of ACF7 leads to aberrant microtubule organization, tight junction stabilization and impaired wound closure in vitro . With the mouse genetics approach, we show that ablation of ACF7 inhibits intestinal wound healing and greatly increases susceptibility to experimental colitis in mice. ACF7 level is also correlated with development and progression of ulcerative colitis (UC) in human patients. Together, our results reveal an important molecular mechanism whereby coordinated cytoskeletal dynamics contributes to cell adhesion regulation during intestinal wound repair and the development of IBD.
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