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METTL14-mediated m6A modification of DUSP6 mRNA participating in postoperative cognitive dysfunction due to
Shengfeng Deng1, Guo Mu1, Jun Li1
1Department of Anesthesiology, Zigong Fourth People's Hospital, Zigong, Sichuan Province 643000, PR China.
Background:
To investigate the mechanisms underlying sevoflurane-induced POCD, C57BL/6 J mice and SH-SY5Y cells were treated with sevoflurane for model establishment.
Methods:
After the treatment with sevoflurane, CCK-8, EdU and flow cytometry were employed to detect cell damage. The levels of N6-methyladenosine (m6A), METTL14 and DUSP6 were determined by qPCR and Western blot. The interaction between METTL14 and DUSP6 was analyzed using RIP-qPCR and Me-RIP methodologies. The cognitive function in mice were assessed by water maze test.
Results:
After sevoflurane treatment, the cell viability, cell proliferation and METTL14 expression were markedly suppressed, while apoptosis was significantly enhanced. METTL14 overexpression elevated the levels of m6A and DUSP6, increased the binding level of METTL14 to DUSP6 mRNA, reducing damage to cells and cognitive dysfunction of mice. Knockdown of DUSP6 negated the beneficial effects observed with METTL14 overexpression.
Conclusion:
Sevoflurane induced POCD by regulating METTL14/DUSP6 through m6A methylation.
Insights
Sevoflurane triggers cognitive dysfunction by altering N6-methyladenosine (m6A) methylation, specifically impacting METTL14 and DUSP6 levels. Restoring these factors mitigates sevoflurane-induced POCD.
Area of Science:
- Neuroscience
- Molecular Biology
- Anesthesiology
Background:
- Postoperative cognitive dysfunction (POCD) is a significant concern following anesthesia.
- Sevoflurane is a commonly used anesthetic agent implicated in POCD.
Purpose of the Study:
- To elucidate the molecular mechanisms behind sevoflurane-induced POCD.
- To investigate the role of N6-methyladenosine (m6A) methylation, METTL14, and DUSP6 in sevoflurane's effects.
Main Methods:
- Establishment of sevoflurane-induced POCD models in C57BL/6J mice and SH-SY5Y cells.
- Assessment of cell viability, proliferation, apoptosis, and m6A levels.
- Analysis of METTL14 and DUSP6 expression and interaction using qPCR, Western blot, RIP-qPCR, and Me-RIP.
- Evaluation of cognitive function in mice via water maze test.
Main Results:
- Sevoflurane treatment suppressed cell viability, proliferation, and METTL14 expression while increasing apoptosis.
- METTL14 overexpression enhanced m6A and DUSP6 levels, reduced cell damage, and improved cognitive function.
- Knockdown of DUSP6 reversed the protective effects of METTL14 overexpression.
Conclusions:
- Sevoflurane induces POCD by modulating the METTL14/DUSP6 pathway via m6A methylation.
- Targeting the METTL14/DUSP6 axis may offer a therapeutic strategy for sevoflurane-induced POCD.
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