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lncRNA Gm16410 Mediates PM2.5-Induced Macrophage Activation via PI3K/AKT Pathway
Jingbin Xu1, Henggui Xu1, Kexin Ma1
1Laboratory Medicine College, Dalian Medical University, Dalian, China.
Abstract:
PM2.5 refers to atmospheric particulate matters with a diameter of less than 2.5 μm. The deposit of PM2.5 in lung cells can cause oxidative stress, leading to changes in macrophage polarity, which can subsequently cause pulmonary inflammation. Long-chain non-coding RNA (lncRNA) is a class of transcripts that regulate biological processes through multiple mechanisms. However, the role of lncRNA in PM2.5-induced lung inflammation has not been established. In this study, the biological effects and associated mechanism of lncRNA in PM2.5-induced change in macrophage polarity were investigated. The lncRNA-mediated PM2.5-induced macrophage inflammation and lung inflammation-associated injury were also determined. Mice were exposed to chronic levels of PM2.5, and changes in the expression of lncRNA in the lung were measured by lncRNA microarray. lncRNAs that showed significant changes in expression in response to PM2.5 were identified. lncRNA showing the biggest change was subjected to further analysis to determine its functional roles and mechanisms with respect to macrophage activation. The result showed that a significant reduction in expression of one lncRNA, identified as lncGm16410, was observed in the lung of mice and RAW264.7 cells following exposure to PM2.5. lncGm16410 suppressed PM2.5-induced macrophage activation via the SRC protein-mediated PI3K/AKT signaling pathway. PM2.5 promoted lung inflammation by downregulating the expression of lncGm16410, enhancing the activation of macrophages. Thus, lncGm16410 might provide new insight into the prevention of PM2.5 injury.
Insights
Exposure to fine particulate matter (PM2.5) causes lung inflammation by altering macrophage polarity. A specific long-chain non-coding RNA (lncRNA), lncGm16410, was found to suppress this inflammation via the PI3K/AKT pathway.
Area of Science:
- Environmental Health
- Molecular Biology
- Immunology
Background:
- Particulate matter (PM2.5) exposure is linked to oxidative stress and pulmonary inflammation.
- Macrophage polarity changes are implicated in PM2.5-induced lung inflammation.
- The role of long-chain non-coding RNAs (lncRNAs) in this process remains unclear.
Purpose of the Study:
- To investigate the biological effects and mechanisms of lncRNAs in PM2.5-induced macrophage polarity changes.
- To determine lncRNA's role in PM2.5-induced macrophage and lung inflammation.
- To identify specific lncRNAs involved in PM2.5-induced lung injury.
Main Methods:
- Mice were exposed to chronic PM2.5 levels.
- lncRNA microarrays were used to measure lncRNA expression changes in lung tissue.
- Functional roles and mechanisms of identified lncRNAs were analyzed in RAW264.7 cells.
Main Results:
- PM2.5 exposure significantly reduced the expression of lncGm16410 in mouse lungs and RAW264.7 cells.
- lncGm16410 suppressed PM2.5-induced macrophage activation through the SRC protein-mediated PI3K/AKT pathway.
- PM2.5 exacerbates lung inflammation by downregulating lncGm16410 and activating macrophages.
Conclusions:
- lncGm16410 plays a protective role against PM2.5-induced lung inflammation.
- The SRC-mediated PI3K/AKT pathway is a key mechanism in lncGm16410's anti-inflammatory effect.
- lncGm16410 represents a potential therapeutic target for preventing PM2.5-related lung injury.
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