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TRIM72 is required for effective repair of alveolar epithelial cell wounding.


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.

SUBMITTER: Kim SC 

PROVIDER: S-EPMC4166787 | biostudies-literature | 2014 Sep

REPOSITORIES: biostudies-literature

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TRIM72 is required for effective repair of alveolar epithelial cell wounding.

Kim Seong Chul SC   Kellett Thomas T   Wang Shaohua S   Nishi Miyuki M   Nagre Nagaraja N   Zhou Beiyun B   Flodby Per P   Shilo Konstantin K   Ghadiali Samir N SN   Takeshima Hiroshi H   Hubmayr Rolf D RD   Zhao Xiaoli X  

American journal of physiology. Lung cellular and molecular physiology 20140808 6


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 i  ...[more]

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