| Literature DB >> 25106429 |
Seong Chul Kim1, Thomas Kellett1, Shaohua Wang2, Miyuki Nishi3, Nagaraja Nagre1, Beiyun Zhou4, Per Flodby4, Konstantin Shilo5, Samir N Ghadiali6, Hiroshi Takeshima3, Rolf D Hubmayr2, Xiaoli Zhao7.
Abstract
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.Entities:
Keywords: acute lung injury; alveolar epithelial cells; caveolin 1; plasma membrane wounding and repair; tripartite motif protein 72
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Year: 2014 PMID: 25106429 PMCID: PMC4166787 DOI: 10.1152/ajplung.00172.2014
Source DB: PubMed Journal: Am J Physiol Lung Cell Mol Physiol ISSN: 1040-0605 Impact factor: 5.464