Fig. 1: Selective deletion of EGFR in myeloid cells led to accelerated functional recovery after ischemic kidney injury and less post-ischemia renal fibrosis. | Nature Communications

Fig. 1: Selective deletion of EGFR in myeloid cells led to accelerated functional recovery after ischemic kidney injury and less post-ischemia renal fibrosis.

From: Myeloid EGFR deficiency accelerates recovery from AKI via macrophage efferocytosis and neutrophil apoptosis

Fig. 1

A Schematic of experimental protocol with IRI-UNX, indicating unilateral pedicle clamping for 28.5 min plus uninephrectomy. B Myeloid EGFR−/− had accelerated functional recovery from the ischemic insult, indicated by more rapid BUN decline (n = 6, 7 and 8). C Myeloid EGFR−/− mouse kidneys had less tubular injury 3 days after injury (n = 6). (D&E) Myeloid EGFR−/− mice had decreased macrophage density, indicated by: D lower mRNA levels of F4/80 (n = 4 and 5) and E quantitative colocalization of CD68 and arginase 1 (ARG1) (n = 4), F Myeloid EGFR−/− mice had lower kidney proinflammatory cytokines/chemokines, including Tnf, Il1a, Il1b, Il6, Ccl2, Ccl3 and Il23a (n = 4 and 5). G–I Myeloid EGFR−/− mice had less kidney fibrosis, indicated by: G lower mRNA (n = 4 and 5) and H protein levels (n = 3 and 4) of profibrotic and fibrotic genes and I less Picrosirius red staining (n = 6) 4 weeks after initial ischemic injury. Scale bar = 50 μm for all. Data are means ± SD (B) or means ± SEM (C–G), *P < 0.05, **P < 0.01, ***P < 0.001, analyzed using 2-way ANOVA followed by Tukey’s post hoc test for (B); 2 tailed Student’s t test (C–I).

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