TRIM72 is required for effective repair of alveolar epithelial cell wounding

Seong Chul Kim, Thomas Kellett, Shaohua Wang, Miyuki Nishi, Nagaraja Nagre, Beiyun Zhou, Per Flodby, Konstantin Shilo, Samir N. Ghadiali, Hiroshi Takeshima, Rolf D. Hubmayr, Xiaoli Zhao

Research output: Contribution to journalArticlepeer-review

19 Scopus citations


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.

Original languageEnglish (US)
Pages (from-to)L449-L459
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Issue number6
StatePublished - Sep 15 2014


  • Acute lung injury
  • Alveolar epithelial cells
  • Caveolin 1
  • Plasma membrane wounding and repair
  • Tripartite motif protein 72

ASJC Scopus subject areas

  • Physiology
  • Pulmonary and Respiratory Medicine
  • Physiology (medical)
  • Cell Biology


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