MOESM3 of Defective angiogenesis in CXCL12 mutant mice impairs skeletal muscle regeneration

Additional file 3: Figure S2. (Related to Figure 2). CXCL12gagtm/gagtm and WT satellite cells show identical behavior. (A) Heat map of the three most up- and down-regulated genes identified by the genome-wide microarray analysis on FACS-sorted SCs from the uninjured TA of WT-Pax7 (n=3) and KI-Pax7 (n=3) mice. Expression of genes is presented as centered and scaled log2 fluorescence intensity (red to yellow key), each row represents a gene, named by its MGI symbol. Confirmation by specific RTqPCRs for the three most up-regulated genes (B) and the three most down-regulated genes (C). Data are represented as the fold change of expression in KI SCs (n=5) compared to WT SCs (n=5) with the use of Wilcoxon signed rank test. SCs from (n=3) WT (Tg:Pax7nGFP) and (n=3) KI (CXCL12Gagtm/Gagtm::Pax7nGFP) were sorted by FACS and plated to assess their behavior by live videomicroscopy: (D) the velocity, (E) the onset first cell division and (F) the division rate. (n=100 cells counted). (G) Quantification by immunostaining 2 days post plating of percentage of MyoD and Pax7 population in WT vs KI SCs and 4 days post plating of percentage of Myogenin and Pax7 population in WT vs KI SCs (n=3 mice per condition and per time point). Data are given as the mean ± SEM. * p < 0.05; ** p < 0.01.