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Inducing Acute Lung Injury in Mice by Direct Intratracheal Lipopolysaccharide Instillation
Published on: July 6, 2019
The 150-kilodalton oxygen-regulated protein ameliorates lipopolysaccharide-induced acute lung injury in mice
Takayuki Nakagomi1, Osamu Kitada, Kozo Kuribayashi
1Department of Internal Medicine, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Hyogo 663-8501, Japan. nakagomi@hyo-med.ac.jp.
Abstract:
The 150-kd oxygen-regulated protein is a novel stress protein that is located in the endoplasmic reticulum and contributes to cell survival when this organelle is under stress. Expression of this protein was strongly increased in alveolar macrophages and alveolar epithelial cells from mice with acute lung injury induced by lipopolysaccharide. Transgenic mice overexpressing the 150-kd protein showed decreased histological severity of this lung injury, accompanied by lower total protein concentrations, and lactate dehydrogenase activity in bronchoalveolar lavage fluid. As indicated by nick end-labeling, lipopolysaccharide induced apoptosis in fewer alveolar wall cells in transgenic than in wild-type mice. Transgenic mice also showed increased survival after lipopolysaccharide injection (a log-rank test). Thus, the 150-kd protein, an endoplasmic reticulum-related molecular chaperone, is pivotal in resisting acute lung injury from lipopolysaccharide.
Insights
The novel 150-kd oxygen-regulated protein, an endoplasmic reticulum chaperone, protects against acute lung injury. Overexpression of this protein enhances survival and reduces lung damage caused by lipopolysaccharide.
Area of Science:
- Cellular stress response
- Molecular biology
- Pulmonary medicine
Background:
- The endoplasmic reticulum is crucial for cell survival under stress.
- Acute lung injury (ALI) involves significant cellular damage.
- Stress proteins play a role in cellular protection.
Purpose of the Study:
- To investigate the role of the 150-kd oxygen-regulated protein in acute lung injury.
- To determine if the 150-kd protein can mitigate lipopolysaccharide-induced lung damage.
Main Methods:
- Studied expression of the 150-kd protein in lipopolysaccharide-induced ALI models.
- Utilized transgenic mice overexpressing the 150-kd protein.
- Assessed histological severity, protein concentration, LDH activity, apoptosis, and survival rates.
Main Results:
- 150-kd protein expression increased in ALI models.
- Overexpression reduced lung injury severity, protein concentration, and LDH activity.
- Apoptosis was decreased, and survival was increased in transgenic mice.
Conclusions:
- The 150-kd protein, an ER-related molecular chaperone, is vital for resisting lipopolysaccharide-induced acute lung injury.
- Targeting this protein may offer a therapeutic strategy for ALI.
