Deficiency of IKKα in Macrophages Mitigates Fibrosis Progression in the Kidney after Renal Ischemia-Reperfusion Injury

Figure 1

Generation of mice with the IKKα gene macrophage-specific ablation and the strategy for the mouse experiment. (a) The strategy of cross-breeding of the IKKα-floxed mice (IKKα fl/fl) with Cre transgenic mice under the control of a lyz2 promoter (lyz2-Cre). Black boxes indicate the exons of the IKKα gene. Orange boxes denote the LoxP sites. (b) PCR analysis for the identification of the genotype of the mice. Lanes 1–3 show the genotyping of the WT mice, while lanes 4–6 indicate the genotypes of Mac IKKα−/− mice. (c) Western blotting demonstrated a significantly reduction in the IKKα protein of macrophages isolated from Mac IKKα−/− mice compared with WT mice after isolation by thioglycollate broth. (d) Strategy for inducing kidney AKI-to-CKD transition: WT and Mac IKKα−/− mice were sacrificed at day 3, day 7, day 14, and day 21 after being subjected to renal IR injury.

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