Mig and its receptor CXCR3 are activated in BM cells after chemotherapy. Normal mice received a single injection of 5-FU (250 mg/kg). (A) BM cells were obtained and counted at different times after 5-FU treatment. Total BM cell counts fell rapidly and reached a minimum on day 7, when BM recovery began. (B left) BM cells pooled from 5 to 20 mice at each time point were used to prepare samples for hybridization to Affymetrix mouse genome expression oligonucleotide arrays. The hybridization intensities of genes encoding Mig, IP-10, I-TAC, and CXCR3 are shown on days 0, 3, 7, 11, and 14 after 5-FU treatment. On day 7, the mig and cxcr3 genes were up-regulated 30- and 6-fold, respectively, compared with baseline (day 0). No significant changes in signal intensities of ip-10 and i-tac were observed. (Right) Plasma levels of ligand protein (determined by ELISA) and receptor expression in BM (determined by FACS). Samples of 3 to 5 mice per time point were individually analyzed for each dot. A 30-fold increase of Mig protein level and more than a 2-fold increase of CXCR3 expression in BMNCs were detected on day 7 (P < .05). There was no change in IP-10 and I-TAC expression. (C) CXCR3 expression of BMNCs, lin⁻ cells, and LSK cells were highly up-regulated during BM regeneration. On day 9 after 5-FU treatment lin⁻ cells and LSK cells were examined for CXCR3 expression in the BM of both nontreated normal mice and treated mice during regeneration. Gray line indicates PE-conjugated isotype control; black line, PE-conjugated anti–mouse CXCR3. Shown is 1 representative result of 3 independent experiments (n = 4-6).