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Visualizing Lung Cellular Adaptations during Combined Ozone and LPS Induced Murine Acute Lung Injury

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Published on: March 21, 2021

TRIM72 mediates lung epithelial cell death upon hyperoxia exposure.

Liang-Ti Huang^1,2, Hsiu-Chu Chou³, Chung-Ming Chen^2,4

¹Department of Pediatrics, Wan Fang Hospital, Taipei Medical University, Taipei, Taiwan, ROC.

Journal of the Chinese Medical Association : JCMA

|August 16, 2020

Summary

Excessive oxygen therapy in premature infants can cause lung injury. This study shows hyperoxia increases tripartite motif protein 72 (TRIM72), leading to cell death and worsening lung damage.

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Isolation of Pulmonary Artery Smooth Muscle Cells from Neonatal Mice

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Published on: October 19, 2013

Area of Science:

Neonatal physiology
Pulmonary medicine
Cellular biology

Background:

Premature infants require oxygen therapy for respiratory distress syndrome, but excessive oxygen can cause bronchopulmonary dysplasia.
Current treatments for bronchopulmonary dysplasia are ineffective.
Tripartite motif protein 72 (TRIM72) plays a role in alveolar epithelial wound repair.

Purpose of the Study:

To investigate the role of TRIM72 in regulating alveolar cells during hyperoxia exposure.
To understand the mechanism of hyperoxia-induced lung injury in neonatal rats.

Main Methods:

In vivo study: Sprague-Dawley rat pups exposed to 85% oxygen for 2 weeks.
Histological analysis of lungs and assessment of TRIM72 expression.
In vitro study: Rat alveolar type II epithelial cells and human lung carcinoma cells exposed to 85% oxygen for 5 days.
Analysis of cell viability and TRIM72 expression.

Main Results:

Hyperoxia exposure reduced body and lung weight and increased lung injury markers.
TRIM72 expression was upregulated in neonatal rat lungs under hyperoxia.
In vitro, TRIM72 modulated lung cell viability, with suppression increasing viability and overexpression decreasing it.

Conclusions:

Hyperoxia upregulates TRIM72 expression in neonatal rat lung tissue.
TRIM72 initiates TRIM72-dependent alveolar epithelial cell death.
TRIM72 plays a critical role in hyperoxia-induced lung injury.