Renal Failure · 2020 · 14 citations · 35 references
MedicineBioinformaticsPathobiologyCell SignalingInflammationRenal PathophysiologyAcute InflammationAcute Kidney InjuryInflammatory SignalingRenal InflammationRenal IschemiaRenal Ischemic InjuryAcute Kidney Injury PathophysiologyCell ActivationHypoxia-reoxygenation InjuryInflammation In Renal InjuryIschemic Acute Kidney InjuryKidney Tissue ModelsLeukocyte Activation SignalingPro-inflammatory Cytokine Expression
Background Krüppel-like factor 6 (KLF6) is a transcription factor that participate in various pathophysiological processes, but its contribution in ischemia acute kidney injury (AKI) is lacking so far. The study aimed to investigate the expression and the role of KLF6 in kidney ischemia–reperfusion (IR) injury.Method Microarray data were collected from GSE58438 and GSE52004. The rat IR model was established to evaluate the mRNA and protein expression of KLF6 and inflammatory cytokines in serum and kidney tissues. SiRNA-KLF6 was transfected with HK-2 cells, and then a cell-based hypoxia-reoxygenation (HR) model was established.Results Bioinformatics showed KLF6 mRNA in kidney tissue is up-regulated in 3 h after IR in rat kidney, which involved in cell activation, leukocyte activation, and response to hydrogen peroxide after IR. The rat IR model results showed that KLF6 expression was peaking at 6 h, and the expression of pro-inflammatory cytokines MCP-1 and TNF-α was increased both in serum and kidney tissues, while anti-inflammatory cytokine IL-10 was decreased after IR. Furthermore, in vitro results showed that KLF6 knock-down reduced the pro-inflammatory cytokines expression.Conclusion These results suggest that (1) KLF6 might be a novel biomarker for early diagnosis of AKI and (2) KLF6 may play a role in promoting inflammation in AKI.
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Distinct Macrophage Phenotypes Contribute to Kidney Injury and Repair
Sik Lee, Sarah C. Huen, Hitoshi Nishio et al. · Journal of the American Society of Nephrology · 2011 · 900 citations · Full text
Medicine, Immunology, Pathobiology +17