CCR2 is critical for homing of inflammatory monocytes to skin wounds. (A) Absolute cell number (left) and fraction of F4/80⁺CD11b⁺ cells (right) in wound tissue of different mutants were determined by FACS analysis (n = 6-10 wounds on 2-5 mice per time point). (B) qRT-PCR analysis for CCL2 in wound tissue from mutants at different time points after injury normalized to unwounded skin. (C) Fractions of SSC^lowCD11b⁺CD115⁺ blood monocytes in unwounded mutants were determined by FACS analysis. (D) Efficiency of LysMCre-mediated CCR2 gene deletion in monocyte precursors/monocytes isolated from BM and blood. Frequency of eGFP⁺ cells within the gate of SSC^lowCD11b⁺CD115⁺ cells isolated from CCR2^wt/flLysMCre mice were determined and correlated with the frequency of eGFP⁺ cells within the gate mentioned above isolated from CCR2^fl/D mice. (E) Representative FACS analysis of PBMCs isolated from CCR2^fl/D mice before and after injury. SSC^lowCD11b⁺CD115⁺ cells were gated and analyzed for the expression of eGFP and Ly6C (n = 3-4 mice per time point). In panels A and B, each dot represents 1 wound; in panels C and D, each dot represents 1 mouse. A minimum of 2 independent experiments were performed and data are expressed as means ± SD. *P < .05; **P < .01; ***P < .001.