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Published on: January 7, 2019
LncRNA NEAT1 activates MyD88/NF-κB pathway in bronchopneumonia through targeting miR-155-5p
Ling-Jia Chen1, Jian-Min Li1, Wei-Dong Zhang1
1Department of Pulmonary and Critical Care Medicine, The First Affiliated Hospital of Hunan Normal University, Hunan Provincial People's Hospital, Changsha, P. R. China.
Background:
Bronchopneumonia is a disease of the respiratory tract. It leads to other complications and endangers life and health. Long non-coding RNA (lncRNA) participates in the occurrence and development of bronchopneumonia. Nuclear paraspeckle assembly transcript 1 (NEAT1) plays a key role in inflammatory diseases, but the function of NEAT1 in bronchopneumonia remains unclear.
Methods:
RT-qPCR and Western blotting were performed to determine genes and proteins expressions. MTT was applied to test cell viability. Cell apoptosis was detected by flow cytometry. RIP was used to investigate the correlation between NEAT1 and miR-155-5p. The interaction between miR-155-5p and NEAT1 or MyD88 was evaluated by the dual-luciferase reporter gene.
Results:
NEAT1 and MyD88 were upregulated in BEAS-2B cells by LPS, while miR-155-5p was downregulated. Knockdown of NEAT1 inhibited LPS-induced BEAS-2B cells growth inhibition by inhibiting the apoptosis. In addition, NEAT1 silencing suppressed LPS-induced inflammatory responses in BEAS-2B cells via suppression of TNF-α, IL-1β, IL-6, and IL-18. Meanwhile, NEAT1 is directly bound to miR-155-5p to regulate MyD88/NF-κB axis, and overexpression of miR-155-5p increased cell proliferation and suppressed inflammatory factors expression levels and cell apoptosis. Furthermore, sh-NEAT1-induced inhibition of BEAS-2B cells injury was partially reversed by miR-155-5p inhibitor or MyD88 overexpression.
Conclusion:
NEAT1 silencing suppressed LPS-induced BEAS-2B cells injury and inflammation by the mediation of miR-155-5p/MyD88/NF-κB axis. Thus, our study might shed new light on exploring the new strategies for the treatment of bronchopneumonia.
Insights
Nuclear paraspeckle assembly transcript 1 (NEAT1) silencing mitigates bronchopneumonia by regulating the miR-155-5p/MyD88/NF-κB pathway. This finding offers potential new therapeutic strategies for treating this respiratory tract infection.
Area of Science:
- Molecular Biology
- Immunology
- Respiratory Medicine
Background:
- Bronchopneumonia is a significant respiratory illness with potential complications.
- Long non-coding RNAs (lncRNAs) are implicated in bronchopneumonia pathogenesis.
- The specific role of Nuclear paraspeckle assembly transcript 1 (NEAT1) in bronchopneumonia was previously unclear.
Purpose of the Study:
- To investigate the function of NEAT1 in bronchopneumonia.
- To elucidate the molecular mechanisms underlying NEAT1's role in this disease.
Main Methods:
- Gene and protein expression analyzed via RT-qPCR and Western blotting.
- Cell viability assessed using MTT assays; apoptosis detected by flow cytometry.
- RNA immunoprecipitation (RIP) and dual-luciferase reporter assays used to confirm molecular interactions.
Main Results:
- NEAT1 and MyD88 were upregulated, while miR-155-5p was downregulated in lipopolysaccharide (LPS)-induced BEAS-2B cells.
- NEAT1 knockdown inhibited cell proliferation, apoptosis, and inflammatory responses (TNF-α, IL-1β, IL-6, IL-18).
- NEAT1 directly targets miR-155-5p, regulating the MyD88/NF-κB axis; miR-155-5p overexpression reversed NEAT1 knockdown effects.
Conclusions:
- NEAT1 silencing ameliorates LPS-induced injury and inflammation in BEAS-2B cells via the miR-155-5p/MyD88/NF-κB pathway.
- This research provides insights into potential novel therapeutic strategies for bronchopneumonia treatment.
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