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Pressure Controlled Ventilation to Induce Acute Lung Injury in Mice
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Inhaled TRIM72 Protein Protects Ventilation Injury to the Lung through Injury-guided Cell Repair.

Nagaraja Nagre1, Xiaofei Cong1, Hong-Long Ji2

  • 11 Department of Physiological Sciences, Eastern Virginia Medical School, Norfolk, Virginia.

American Journal of Respiratory Cell and Molecular Biology
|June 30, 2018
PubMed
Summary

Inhaled recombinant human TRIM72 protein (rhT72) protects lung tissue from ventilator injury by enhancing cell membrane repair and resilience. This protein accumulates in injured lungs, improving outcomes in models of lung damage.

Keywords:
acute respiratory distress syndromebiomarkerscell injury and repairtripartite motif–containing protein 72ventilator-induced lung injury

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Area of Science:

  • Biomedical Engineering
  • Cell Biology
  • Pulmonary Medicine

Background:

  • TRIM72 protein is crucial for repairing alveolar cell membrane damage.
  • Exogenous recombinant human TRIM72 (rhT72) shows tissue-mending capabilities in animal injury models.

Purpose of the Study:

  • To investigate the mechanisms of rhT72-mediated lung cell protection in vitro.
  • To evaluate the efficacy of inhaled rhT72 in mitigating ventilator-induced lung injury (VILI) in mice.

Main Methods:

  • In vitro cell injury induced by glass beads and stretching.
  • VILI modeled using injurious ventilation; rhT72 administered via nebulization.
  • Cellular uptake and distribution of rhT72 assessed using imaging and immunostaining.

Main Results:

  • rhT72 dose-dependently maintained alveolar epithelial cell membrane integrity against glass bead injury.
  • Inhaled rhT72 reduced fatally injured alveolar cells and ameliorated VILI indicators.
  • rhT72 enhanced cellular resilience to membrane wounding and improved post-injury repair.

Conclusions:

  • Inhaled rhT72 accumulates in injured lungs and protects against VILI.
  • Mechanisms involve enhanced cell membrane resilience, localization to injury sites, and augmented repair.
  • rhT72 uptake by alveolar cells is cholesterol-dependent and targets wounded membranes.