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. Author manuscript; available in PMC: 2009 Jun 1.
Published in final edited form as: Kidney Int. 2008 Oct 8;74(12):1526–1537. doi: 10.1038/ki.2008.500

Figure 4. CCR2-deficient signaling protects kidneys from IRI. (a, c, d).

Figure 4

WT mice (CCR2+/+) and age-, weight-, and gender-matched CCR2−/− mice and (b, e, f) CCR2+/+ → CCR2+/+, CCR2−/− → CCR2+/+ BM chimera mice were subjected to 32 min of ischemia followed by 24 h of reperfusion. Plasma creatinine is shown in (a, b). Values are mean ± s.e.; N = 4–11; **P < 0.001. (c–f) H&E staining of kidney outer medulla is shown. There was more tubule cell injury and necrosis after IRI in WT (CCR2+/+) and CCR2+/+ → CCR2+/+ BM chimera mice (c, e, right). However, IRI kidneys from CCR2−/− mice and CCR2−/− → CCR2+/+ BM chimera mice were protected from IRI (d, f, right). The arrows are pointing to the necrotic tubules in (c, e, right). Magnification, × 200. (g) Recruitment of F4/80low macrophages in kidneys of CCR2−/−, CCR2+/+, CCR2+/+ → CCR2+/+, and CCR2−/− → CCR2+/+ chimera mice following 24 h reperfusion compared with controls. Values are mean ± s.e.; N = 4–10; *P < 0.05; **P < 0.001; NS, not significant.