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. Author manuscript; available in PMC: 2021 Sep 1.
Published in final edited form as: Kidney Int. 2019 Nov 28;97(5):966–979. doi: 10.1016/j.kint.2019.11.013

Figure 9. Hepatocyte-specific Lcn2 (NGAL) deficient mice have reduced plasma and urine NGAL after ischemic AKI.

Figure 9.

Normal mice (no procedure), sham (surgery alone) and ischemic AKI were studied in hepatocyte specific Lcn2 deficient (Lcn2hep−/−) mice, Cre-negative floxed littermates were used as controls (Lcn2hep+/+). (A, B, C) Plasma and urine NGAL were dramatically reduced in Lcn2Hep−/− versus Lcn2Hep+/+. As expected, Liver mRNA NGAL expression was decreased in Lcn2hep−/− versus Lcn2Hep+/+; NGAL mRNA was similar in the (B) kidney and (C) lung in Lcn2Hep−/− versus Lcn2Hep+/+; (D) spleen mRNA NGAL was reduced after AKI in Lcn2Hep−/− versus Lcn2Hep+/+. NGAL protein levels were reduced in Lcn2hep−/− Lcn2Hep−/− versus Lcn2Hep+/+ in the (E) liver, and (K) kidney, but not the lung and spleen in AKI. Kidney function with AKI was similar as judged by (L) BUN, (M) plasma creatinine and (N) kidney mRNA KIM-1 expression. (O) Plasma 1L-6 levels were similar in AKI. Results are expressed as mean ±SEM; N = 4-6 mice per group from 3 exDeriments. Analyzed by t test. *P < 0.05. **P < 0.01 and ***P < 0.001, Lcn2hep+/+ vs. Lcn2hep−/−.