Fig. 7: Slug is an SDF1α downstream effector during angiogenesis.

a SDF1α treatment leads to early and increased tip cell formation and sprouting in the fibrin-gel bead assay. Scale bar: 100 µm. b SDF1α treatment leads to activation of Snai2 but not Snai1 transcription (n ≥ 3 cell lines per condition, see source data for detail. 24 h p = 0.04, 48 h p = 0.012, and 72 h p = 0.003). c SDF1α induces increased sprouting in WT (p = 0.003) but not SlugKO mouse retina explants. Scale bar: 100 µm. d Quantification of the number of sprouts per retina explant (WT-Ctrl n = 12 animals, WT-SDF1α n = 10 animals, SlugKO-Ctrl n = 9 animals, SlugKO-SDF1α n = 11 animals). e qPCR analysis of Slug induction by SDF1α in EC treated with siCtrl (n = 4 cell lines, p = 0.0002), siCXCR4 (n = 3 cell lines, p = 0.004), or siCXCR7 (n = 4 cell lines, p = 0.001). f Slug overexpression in EC rescues AMD3100 inhibition of sprouting. (n = 3 cell lines for all conditions, p = 0.0057). g SDF1α activation of ERK5 phosphorylation and blocking by inhibition of ERK5 (XMD8-92) or CXCR4 (AMD3100). h ERK5 phosphorylation downstream of SDF1α is abolished by CXCR4 knockdown but not CXCR7 knockdown. i SDF1α induction of Slug (p = 0.0037) is blocked by the ERK5 inhibitor XMD8-92 (n = 4 cell lines for all conditions). j Model for Slug-mediated pathological angiogenesis. Data represent mean ± SEM. Two-tailed unpaired equal-variance t-test. *p < 0.05, **p < 0.01, ***p < 0.005. Source data are provided as a Source Data file.