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http://purl.uniprot.org/citations/30157481http://www.w3.org/1999/02/22-rdf-syntax-ns#typehttp://purl.uniprot.org/core/Journal_Citation
http://purl.uniprot.org/citations/30157481http://www.w3.org/2000/01/rdf-schema#comment"

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-κB and AKT pathways were both activated. The pre-treatment of microRNA-138 inhibitor decreased inflammatory factors, downregulated the NF-κB 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-κB pathway."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.org/dc/terms/identifier"doi:10.1159/000492988"xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Han F."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Liu Y."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Shi J.H."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Zhang W."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Cao M.Y."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Zhang J.L."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Wang K.J."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Li X.Q."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Zhang J.N."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Hu D.H."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/author"Bai X.Z."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/date"2018"xsd:gYear
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/name"Cell Physiol Biochem"xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/pages"489-500"xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/title"MicroRNA-138 Aggravates Inflammatory Responses of Macrophages by Targeting SIRT1 and Regulating the NF-kappaB and AKT Pathways."xsd:string
http://purl.uniprot.org/citations/30157481http://purl.uniprot.org/core/volume"49"xsd:string
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