Open AccessTRIM72 is required for effective repair of alveolar epithelial cell wounding
Author(s) -
Seong Chul Kim,
Thomas Kellett,
Shaohua Wang,
Miyuki Nishi,
Nagaraja N. Nagre,
Baosen Zhou,
Per Flodby,
Konstantin Shilo,
Samir N. Ghadiali,
Hiroshi Takeshima,
Rolf D. Hubmayr,
Xiaoli Zhao
Publication year - 2014
Publication title -
american journal of physiology. lung cellular and molecular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.892
H-Index - 163
eISSN - 1522-1504
pISSN - 1040-0605
DOI - 10.1152/ajplung.00172.2014
Subject(s) - microbiology and biotechnology , propidium iodide , a549 cell , cell , biology , lung , pathology , apoptosis , programmed cell death , medicine , biochemistry
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.