AI Article Synopsis
- This study investigates the effects of Re on liver ischemia-reperfusion injury (IRI) using a human liver cell line exposed to hypoxia and reperfusion conditions.
- Re treatment was found to reduce cell apoptosis and enhance cell viability, while also lowering the levels of METTL3 and m6A, which were elevated during H/R treatment.
- The findings suggest that the Re-METTL3-P53 pathway plays a crucial role in mitigating liver IRI, indicating a potential therapeutic direction for future treatment strategies.
Article Abstract
Background: This study was performed to explore the role of Re in liver IRI progression. Hypoxia and reperfusion (H/R) treated human embryo liver cell line (L-02) was used to establish a liver IRI model.
Materials And Methods: Cell behaviors were detected using CCK-8, flow cytometry and TUNEL staining assays. The m6A content was detected using m6A dot blot assay. RT-qPCR and western blot assays were used to assessed the relative mRNA and protein levels. MeRIP assay was conducted to determine the m6A levels of P53. The relationship between METTL3 and P53 was demonstrated using RIP and dual-luciferase reporter assays.
Results: The results showed that Re treatment significantly decreased the cell apoptosis and promoted the cell viability in the H/R treated L-02 cells. Besides, H/R treatment increased the METTL3 and m6A levels in the L-02 cells, and Re treatment decreased them. Additionally, METTL3 overexpression reversed the role of Re in the H/R treated L-02 cells. Mechanistically, METTL3 overexpression enhanced the m6A levels and mRNA stability and expressions of P53. The combination of METTL3 and P53 was further confirmed.
Conclusion: In conclusion, this study demonstrated that Re treatment relieved the H/R induced injury in the L-02 cells through decreasing the METTL3 levels. METTL3 enhanced the mRNA stability and expressions of P53 through m6A modification. Re-METTL3-P53 axis might a new direction for the treatment of liver IRI in the future.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC10560062 | PMC |
| http://dx.doi.org/10.1016/j.heliyon.2023.e20285 | DOI Listing |
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