Fig. 8: EGFR signaling promoted renal neutrophil survival via maintaining antiapoptotic protein Mcl-1 levels after ischemic injury. | Nature Communications

Fig. 8: EGFR signaling promoted renal neutrophil survival via maintaining antiapoptotic protein Mcl-1 levels after ischemic injury.

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

Fig. 8: EGFR signaling promoted renal neutrophil survival via maintaining antiapoptotic protein Mcl-1 levels after ischemic injury.The alternative text for this image may have been generated using AI.

NeutEGFR−/− and WT mice underwent ischemic injury and were sacrificed at the indicated time points. A Three days after ischemic injury, expression of both p-EGFR and Mcl-1 in kidney neutrophils was evident in WT mice but was minimal in NeutEGFR−/− mice. B–D After ischemic injury, the number of Mcl-1 expressing neutrophils was comparable between WT and NeutEGFR−/− mice at 2 h and 6 h but was markedly lower at 16 and 72 h in NeutEGFR−/− mice (n = 5–8). E In isolated WT bone marrow neutrophils EGF administration for 16 h induced immunoreactive Mcl-1 protein, which was markedly attenuated in EGFR−/− bone marrow neutrophils isolated from myeloid EGFR−/− mice. Scale bar = 50 μm for all. Data are means ± SD, **P < 0.01, ***P < 0.001, analyzed using 2-way ANOVA followed by Tukey’s post hoc test.

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