The lncRNA CASC9 alleviates lipopolysaccharide-induced acute kidney injury by regulating the miR-424-5p/TXNIP pathway
Autor: | Chun-Wen Guo, Hong Yan, Yu-Tang Li, Hai-Peng Fan, Zhi-Xia Zhu, Jia-Jun Xu |
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Jazyk: | angličtina |
Rok vydání: | 2021 |
Předmět: |
Lipopolysaccharides
Medicine (General) antioxidant Thioredoxin-Interacting Protein Lipopolysaccharide Inflammation Biochemistry Pre-Clinical Research Report chemistry.chemical_compound Mice Thioredoxins R5-920 Sepsis Medicine cancer susceptibility candidate 9 Animals Humans sepsis-related acute kidney injury thioredoxin-interacting protein business.industry Biochemistry (medical) lipopolysaccharide Acute kidney injury apoptosis RNA Cell Biology General Medicine Acute Kidney Injury medicine.disease miR-424-5p Long non-coding RNA MicroRNAs chemistry Apoptosis inflammation Cancer research RNA Long Noncoding medicine.symptom business Carrier Proteins TXNIP |
Zdroj: | Journal of International Medical Research, Vol 49 (2021) The Journal of International Medical Research |
ISSN: | 1473-2300 |
Popis: | Objective This study aimed to clarify the mechanism by which the long non-coding RNA cancer susceptibility candidate 9 (CASC9) alleviates sepsis-related acute kidney injury (S-AKI). Methods A lipopolysaccharide (LPS)-induced AKI model was established to simulate S-AKI. HK-2 human renal tubular epithelial cells were treated with LPS to establish an in vitro model, and mice were intraperitoneally injected with LPS to generate an in vivo model. Subsequently, the mRNA expression of inflammatory and antioxidant factors was validated by quantitative reverse transcription polymerase chain reaction (RT-qPCR). Reactive oxygen species (ROS) production was assessed using an assay kit. Apoptosis was detected by western blotting and fluorescence-activated cell sorting. Results CASC9 was significantly downregulated in the LPS-induced AKI model. CASC9 attenuated cell inflammation and apoptosis and enhanced the antioxidant capacity of cells. Regarding the mechanism, miR-424-5p was identified as the downstream target of CASC9, and the interaction between CASC9 and miR-424-5p promoted thioredoxin-interacting protein (TXNIP) expression. Conclusions CASC9 alleviates LPS-induced AKI in vivo and in vitro, and CASC9 directly targets miR-424-5p and further promotes the expression of TXNIP. We have provided a possible reference strategy for the treatment of S-AKI. |
Databáze: | OpenAIRE |
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