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Published on: May 2, 2018
Increased susceptibility of MER5 (peroxiredoxin III) knockout mice to LPS-induced oxidative stress
Lianqin Li1, Wataru Shoji, Hirohisa Takano
1Department of Cell Biology, Institute of Development, Aging, and Cancer, Tohoku University, 4-1 Seriyo-machi, Aoba-ku, Sendai 980-8575, Japan.
Abstract:
MER5 (also called peroxiredoxin III, PrxIII) is a member of peroxiredoxin family that has antioxidant activity. The present study was performed to investigate its in vivo function using MER5 knockout mice. MER5 knockout mice were born in normal frequency and could grow to maturity, but we found that intracellular ROS levels are significantly higher in the macrophages of the knockout mice. We examined roles of MER5 function for the oxidative stress responses by intratracheal inoculation of lipopolysaccharide (LPS) to the mice. Lung inflammation such as inflammatory cell infiltration and airway wall thickening was more severely detected in the knockout mice. At the same time, oxidative damage on DNA and proteins was more strongly detected in lung tissues of the knockout mice, including 8-hydroxy-2'-deoxyguanosine (8-OHdG) formation and protein carbonylation. The degrees of lung inflammation and oxidative damage were positively related with LPS doses. Our results indicate that MER5 knockout mice accumulated higher intracellular ROS levels, which cause LPS-induced lung injury more severely, and thus, suggested that MER5 acts as an important scavenger of reactive oxygen species (ROS) under oxidative stress.
Insights
Mice lacking the antioxidant MER5 (peroxiredoxin III) showed higher reactive oxygen species (ROS) levels. This deficiency led to more severe lung inflammation and oxidative damage following lipopolysaccharide exposure.
Area of Science:
- Biochemistry
- Immunology
- Cell Biology
Background:
- The peroxiredoxin family, including MER5 (peroxiredoxin III), possesses antioxidant properties.
- Understanding the in vivo function of MER5 is crucial for elucidating its role in oxidative stress responses.
Purpose of the Study:
- To investigate the in vivo function of MER5 using knockout mouse models.
- To determine the role of MER5 in mitigating oxidative stress and inflammation.
Main Methods:
- Generation and characterization of MER5 knockout mice.
- Intratracheal inoculation of lipopolysaccharide (LPS) to induce lung inflammation.
- Assessment of intracellular reactive oxygen species (ROS) levels, lung inflammation markers, and oxidative damage (8-OHdG, protein carbonylation).
Main Results:
- MER5 knockout mice exhibited significantly higher intracellular ROS levels in macrophages.
- These mice showed exacerbated LPS-induced lung inflammation, including increased inflammatory cell infiltration and airway wall thickening.
- Enhanced oxidative damage to DNA and proteins was observed in the lungs of MER5 knockout mice, correlating positively with LPS dosage.
Conclusions:
- MER5 plays a critical role in scavenging reactive oxygen species (ROS) under oxidative stress conditions.
- The absence of MER5 leads to increased susceptibility to LPS-induced lung injury due to elevated ROS accumulation.
- MER5 is a key protective factor against oxidative stress-mediated lung inflammation.
