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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 10. Ly6G+ cells are not the source of plasma or urine NGAL after ischemic acute kidney injury (AKI).

Figure 10.

Normal mice (Nl), and mice with and without depletion of Ly6G+ cells were studied 4 and 24 hours after ischemic AKI. Ly6G is predominantly expressed on neutrophils. There was no change in kidney function/injury after AKI with Ly6G+ cell depletion as judged by (A) BUN, (B) plasma creatinine and (C) kidney Kim1 mRNA. Neither (D) plasma nor (E,F) urine NGAL were affected by Ly6G+ cell depletion. (G) Liver, (H) kidney, (I) spleen, and (J) lung NGAL production was not affected by Ly6G+ depletion. NGAL protein levels in the liver and kidney (K and L) were not affected by Ly6G+ cell deletion. NGAL protein was reduced in the spleen at 24 hours in the lung at 4 and 24 hours after AKI with Ly6G+ cell depletion (N). Neutrophil depletion was confirmed by flow cytometry of the spleen (O). Results are expressed as mean ±SEM; 2 separate experiments. Analyzed by t test, Ly6G+ versus Ly6G− at the same time point. (N=4-10)