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. Author manuscript; available in PMC: 2009 Dec 15.
Published in final edited form as: J Immunol. 2008 Dec 15;181(12):8670–8676. doi: 10.4049/jimmunol.181.12.8670

Figure 1. CCL3 (MIP-1α) and CCL5 (RANTES) expression are upregulated after renal ischemia-reperfusion injury.

Figure 1

Protein levels of CCL3 (MIP-1α) (A) and CCL5 (RANTES) (B) were detected by ELISA. −/−, CCR1 knockout mice; +/+, wild type C57BL/6 control mice; sham, sham-operated wild type C57BL/6 mice tested one day after surgery. Shown are summary data presented as mean ± SEM from 3 independent experiments with 3–5 mice in each experiment. Panel C part i and ii, ischemia-reperfusion injured kidney from wild type C57BL/6 mouse 4 days after injury stained with anti-CCL3 (MIP-1α) and control IgG, respectively. Tissue was counterstained with hematoxylin. Original magnification of all images is 320X. Panel D part i and ii, ischemia-reperfusion injured kidney from wild type C57BL/6 mouse 4 days after injury stained with anti-F4/80, and anti-CCL3 (MIP-1α), respectively. D part iii is a merged picture of part i and ii. Original magnification of all images is 400X. Scale bar indicates 50µm. * P<0.05 comparing CCR1-deficient mice versus wild type mice at the same time point.