Journal
CELLULAR PHYSIOLOGY AND BIOCHEMISTRY
Volume 49, Issue 2, Pages 489-500Publisher
KARGER
DOI: 10.1159/000492988
Keywords
Inflammation; MicroRNA-138; SIRT1; Macrophage; NF-kappa B; AKT
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Funding
- National Natural Science Foundation of China [81501663, 81501666, 81530064]
- Burns Center of PLA, Department of Burns and Cutaneous Surgery, Xijing Hospital
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Background/Aims: With increased understanding of sepsis, mortality is decreasing. However, there is still a lack of effective therapeutic strategy. The inflammatory response of macrophages is critical during sepsis. Methods: Macrophages were stimulated with LPS. Western blotting and qRT-PCR were used to detect inflammatory responses. Then, the inhibitor of microRNA-138 was transfected and Western blotting, qRT-PCR, H&E staining and ELISA were used to verify the role of microRNA-138 in inflammation. Then target gene prediction databases were used to predict the potential target of microRNA-138. Both animal and cell models under LPS challenges were established to verify the regulation of SIRT1 and microRNA-138 during inflammation. Results: The present study showed that microRNA-138 was increased in macrophages stimulated with LPS. Additionally, the NF-kappa B and AKT pathways were both activated. The pre-treatment of microRNA-138 inhibitor decreased inflammatory factors, downregulated the NF-kappa B pathway, activated the AKT pathway and protected against organ damage in mice challenged with LPS. SIRT1 was demonstrated as a potential target of microRNA-138In macrophages stimulated with LPS, the inhibition effect of microRNA-138 inhibitor on inflammation was lost by SIRT1 siRNA pre-treatment. In the animal model, the protective effect of microRNA-138 antagomir disappeared in SIRT1 knockout mice. Conclusion: We demonstrated that miR-138 participated in the inflammatory process by inhibiting SIRT1 and activating the NF-kappa B pathway. (c) 2018 The Author(s) Published by S. Karger AG, Basel
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