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METTL3 promotes inflammation and cell apoptosis in a pediatric pneumonia model by regulating EZH2
Ying Yang1, Xiaoqing Yang2, Yi Wu3
1Department of Pediatrics, Women and Children's Hospital, School of Medicine, Xiamen University, Xiamen, Fujian China.
Background:
In recent times, the medical science has developed by leaps and bounds, however, the molecular mechanism of pediatric pneumonia is still unclear. Although prior researches have shown that methyltransferase-like 3 (METTL3) is up-regulated in a variety of inflammatory diseases, its role and mechanism has been rarely studied in pediatric pneumonia, and need to be defined elaborately.
Objective:
In this study, the related molecular mechanism of METTL3 on inflammation and cell apoptosis in a pediatric pneumonia was investigated.
Materials And Methods:
Quantitative real-time polymerase chain reaction (qPCR) and western blot assays were employed to examine the mRNA and protein expression level of METTL3 and EZH2 in peripheral blood monocytes from pediatric pneumonia patients or cell model (WI-38). Then, qPCR and ELISA assay were applied to verify the inflammatory response in LPS-treated WI-38 cell lines after knockdown of METTL3. Besides, MTT cell viability assays, flow cytometry, and western blot assays were applied to examine the cell viability and cell apoptosis of LPS-treated WI-38 cell after knockdown of METTL3. Further, the western blot assays were employed to examine the protein expression levels of p-JAK2, JAK2, p-STAT3, STAT3, and EZH2 in LPS-treated WI-38 cell after knockdown of METTL3. Finally, ELISA and western blot were applied to verify the inflammatory response and cell apoptosis of LPS-treated WI-38 cell after knockdown of METTL3 and overexpression of EZH2.
Results:
In this study, the results showed that METTL3 and EZH2 were highly expressed in pediatric pneumonia patients and cell models (WI-38), respectively. Besides, downregulation of METTL3 inhibited LPS-induced inflammatory response and cell apoptosis. Then, the fact that METTL3 regulates the JAK2/STAT3 signaling pathway through EZH was proved. Furthermore, downregulation of METTL3 inhibits inflammation and apoptosis through EZH2.
Conclusion:
This study found that METTL3 promotes inflammation and cell apoptosis in a pediatric pneumonia model by regulating EZH2.
Insights
Methyltransferase-like 3 (METTL3) promotes pediatric pneumonia by increasing inflammation and cell apoptosis. Downregulating METTL3 inhibits these effects by regulating EZH2 and the JAK2/STAT3 pathway.
Area of Science:
- Molecular Biology
- Immunology
- Pediatrics
Background:
- The molecular mechanisms underlying pediatric pneumonia remain largely unclear.
- Methyltransferase-like 3 (METTL3) is implicated in inflammatory diseases, but its specific role in pediatric pneumonia requires elucidation.
Purpose of the Study:
- To investigate the molecular mechanism of METTL3 in pediatric pneumonia, focusing on inflammation and cell apoptosis.
- To explore the role of METTL3 in regulating the JAK2/STAT3 signaling pathway and its interaction with EZH2.
Main Methods:
- Quantitative real-time PCR and Western blot to assess METTL3 and EZH2 expression in patient samples and cell models.
- ELISA and MTT assays to evaluate inflammatory responses, cell viability, and apoptosis in LPS-treated cells with altered METTL3 levels.
- Analysis of JAK2/STAT3 pathway activation following METTL3 modulation.
Main Results:
- METTL3 and EZH2 were found to be highly expressed in pediatric pneumonia patients and cell models.
- Downregulation of METTL3 significantly inhibited lipopolysaccharide (LPS)-induced inflammation and cell apoptosis.
- METTL3 was demonstrated to regulate the JAK2/STAT3 signaling pathway via EZH2, thereby influencing inflammation and apoptosis.
Conclusions:
- METTL3 plays a crucial role in promoting inflammation and cell apoptosis in pediatric pneumonia.
- Targeting METTL3, potentially through its regulation of EZH2, offers a promising therapeutic strategy for pediatric pneumonia.
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