Fig. 8. CXCL12-CXCR4 signaling contributes to the migration of cells from the SVZ to peri-infarct cortex.

a Fluorescence images showing upregulation of the chemokine CXCL12 in peri-infarct cortex. b Quantification of CXCL12 fluorescence intensity in contralateral and peri-infarct cortex 7 days post-stroke. *t(4) = 4.2. p = 0.014, two-tailed t test. N = 3 mice. c Immunostaining revealed strong expression of CXCL12 in peri-infarct vasculature (labeled with tomato lectin), but not astrocytes (labeled with GFAP). Images are representative of experiments conducted in n = 3 mice. d Confocal images and quantification showing that lineage traced cells migrating from the SVZ to peri-infarct cortex express the CXCL12 receptor CXCR4. n = 3 mice. e Experimental timeline for antagonizing CXCR4. f Images of lineage traced cells migrating from the SVZ to peri-infarct cortex 14 days post-stroke in mice treated with Plerixafor or vehicle. g Treatment with the CXCR4 antagonist Plerixafor significantly reduced the number of SVZ-derived cells that migrated to peri-infarct cortex. *t(10) = 7.4. p < 0.0001, two-tailed t test. N = 6 Nestin^CreERT2; Ai14 mice per group. Data are presented as mean ± SEM. Where individual datapoints are shown, datapoints representing males are shown as circles; datapoints representing females are shown as squares. Source data are provided as a Source Data file.