TRIM72 is required for effective repair of alveolar epithelial cell wounding
TRIM72 is required for effective repair of alveolar epithelial cell wounding
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DOI：
10.1152/ajplung.00172.2014
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发表时间：
2014-09-15
影响因子：
4.9
通讯作者：
Zhao, Xiaoli
中科院分区：
文献类型：
--
作者：
Kim, Seong Chul;Kellett, Thomas;Zhao, Xiaoli
肺细胞修复的分子机制在很大程度上是未知的。先前的研究从横纹肌中鉴定了三重基序蛋白72（TRIM72），并将其功能与组织修复联系起来。在这项研究中，我们表征了TRIM72在肺组织中的表达，并研究了TRIM72在肺泡上皮细胞修复中的作用。在体内肺细胞损伤的高潮气量通气，修复缺陷的细胞被标记与损伤后管理的碘化丙啶。分离原代肺泡上皮细胞，分别标记膜损伤和膜修复。我们的研究结果表明，TRIM72的缺乏增加了对变形诱导的肺损伤的易感性，而TRIM72过表达是保护性的。体外细胞损伤实验表明，TRIM72通过促进修复而不是增加对损伤的抵抗力来保护肺泡上皮细胞。TRIM72在肺细胞中的修复功能进一步与小窝蛋白1相关。这些数据表明TRIM72在质膜应激衰竭下的肺泡上皮细胞修复中的重要作用。
The molecular mechanisms for lung cell repair are largely unknown. Previous studies identified tripartite motif protein 72 (TRIM72) from striated muscle and linked its function to tissue repair. In this study, we characterized TRIM72 expression in lung tissues and investigated the role of TRIM72 in repair of alveolar epithelial cells. In vivo injury of lung cells was introduced by high tidal volume ventilation, and repair-defective cells were labeled with postinjury administration of propidium iodide. Primary alveolar epithelial cells were isolated and membrane wounding and repair were labeled separately. Our results show that absence of TRIM72 increases susceptibility to deformation-induced lung injury whereas TRIM72 overexpression is protective. In vitro cell wounding assay revealed that TRIM72 protects alveolar epithelial cells through promoting repair rather than increasing resistance to injury. The repair function of TRIM72 in lung cells is further linked to caveolin 1. These data suggest an essential role for TRIM72 in repair of alveolar epithelial cells under plasma membrane stress failure.