MOESM4 of Defective angiogenesis in CXCL12 mutant mice impairs skeletal muscle regeneration

Additional file 4: Figure S3. (Related to Figure 2). KI ECs display an increased angiogenic response. (A) Heat map of the three most up- and down-regulated genes identified by the genome-wide microarray analysis on FACS-sorted ECs from the uninjured TA of WT-Flk1 (n=3) and KI-Flk1 (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 ECs (n=5) compared to WT ECs (n=5) with the use of Wilcoxon signed rank test. (D) Representative immunostaining of matrigel plugs mixed with KI (CXCL12Gagtm/Gagtm::Pax7nGFP) satellite cells inserted for 3 weeks in KI (CXCL12Gagtm/Gagtm) mice with endothelial cells (CD31, red) and myoblasts (Desmin, green). Scale bars represent 10 μm. (E) Quantification of the CD31 positive/negative surface ratio in matrigel plugs mixed with the KI (CXCL12Gagtm/Gagtm::Pax7nGFP) or the WT (Tg:Pax7nGFP) SCs inserted for 3 weeks in either the WT (C57Bl6) or the KI (CXCL12Gagtm/Gagtm) mice. Data are mean percentage ± SEM (10 fields per matrigel plug). Five animals (n=5) were used per condition and were repeated independently two times. Data are given as the mean ± SEM.* p < 0.05; ** p < 0.01.