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Endothelial Microparticles Derived from Primary Pulmonary Microvascular Endothelial Cells Mediate Lung Inflammation
Yiming Ma1, Xue He1, Xiangming Liu1
1Department of Respiratory and Critical Care Medicine, The Second Xiangya Hospital of Central South University, Changsha, People's Republic of China.
Background:
Extracellular vesicles (EVs) are considered to new types of intercellular communication media, and microRNA is one of the most common transferring components of EVs. This study aimed to explore the potential role of endothelial microparticles (EMPs) derived from primary pulmonary microvascular endothelial cells in regulating lung inflammation of chronic obstructive pulmonary disease (COPD) through transferring microRNA-126 (miR-126).
Methods:
EMPs generated from primary pulmonary microvascular endothelial cells were isolated by gradient centrifugation and characterized by transmission electron microscopy, flow cytometry and Western blotting. EMPs were treated to in vitro and in vivo COPD models induced by cigarette smoke extract (CSE). miR-126 mimics or inhibitors were transfected into EMPs by calcium chloride. Pathological changes of lung tissue, mRNA and protein levels of inflammation-related factors were measured to explore the effect of EMPs transferring miR-126 on CSE-induced inflammation.
Results:
Both in vitro and in vivo studies demonstrated that mRNA and protein levels of inflammation-related factors were significantly increased in COPD group, while EMPs could dramatically reverse these increases. In vitro, overexpression of miR-126 in EMPs decreased HMGB1 expression and magnified the decreasing effect of EMPs on inflammation-related factors.
Conclusion:
The present study reveals that EMPs are capable of alleviating lung inflammation and transferring miR-126 can magnify the anti-inflammatory effect of EMPs, which may provide a novel therapeutic alternative for COPD.
Insights
Endothelial microparticles (EMPs) transfer microRNA-126 to reduce lung inflammation in chronic obstructive pulmonary disease (COPD). This suggests EMPs and miR-126 offer a new therapeutic approach for COPD patients.
Area of Science:
- Cellular Biology
- Immunology
- Pulmonary Medicine
Background:
- Extracellular vesicles (EVs) mediate intercellular communication, with microRNAs being key cargo.
- Endothelial microparticles (EMPs) from pulmonary microvascular cells are investigated for their role in lung inflammation.
- Chronic obstructive pulmonary disease (COPD) involves significant lung inflammation.
Purpose of the Study:
- To investigate the role of EMPs in regulating lung inflammation in COPD.
- To determine if EMPs transfer microRNA-126 (miR-126) and if this impacts COPD inflammation.
- To explore EMPs as a potential therapeutic strategy for COPD.
Main Methods:
- EMPs were isolated from primary pulmonary microvascular endothelial cells and characterized.
- In vitro and in vivo COPD models induced by cigarette smoke extract (CSE) were used.
- miR-126 mimics/inhibitors were transfected into EMPs, and inflammatory markers were assessed.
Main Results:
- EMPs significantly reversed CSE-induced increases in inflammation-related factors in lung tissue.
- Overexpression of miR-126 in EMPs enhanced the anti-inflammatory effects.
- EMPs transferring miR-126 reduced HMGB1 expression in vitro.
Conclusions:
- EMPs alleviate lung inflammation associated with COPD.
- Transferring miR-126 amplifies the anti-inflammatory capacity of EMPs.
- EMPs represent a potential novel therapeutic alternative for COPD treatment.
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