GSE202753
DsbA-L deficiency attenuates LPS-induced acute kidney injury via NF-?B/AP-1 regulation of macrophage polarization
Background: Disulfide bond A oxidoreductase-like protein (DsbA-L) drives acute kidney injury (AKI) progression in proximal tubular cells by directly upregulating voltage-dependent anion-selective channel levels; however, its role in immune cells remains unclear.  Methods: We used the mouse model of AKI induced by LPS to explore the mechanism of how DsbA-L deficiency regulating macrophages and kidney injury under the guidance of transcriptome and metabolic.  Results: DsbA-L knockout resulted in significant changes in the JNK pathway, which might affect macrophage polarization to reduced AKI injury based on the cellular and stimulus-dependent characteristics of JNK function Overall design: The mice were divided into four groups: naïve-WT, naïve-DsbA-L-/-, LPS-WT and LPS-DsbA-L-/- (n = 3-6 mice in each group). Each mouse in the naïve and experimental groups was intraperitoneally injected with 200 µL saline and 10 mg/kg LPS (Sigma-Aldrich, USA, L2630), respectively.