Fig. 4

Equipotent inhibition of spontaneous and FGF-2-induced HMVEC migration by intact CXCL10_(1–77) or C-terminally truncated CXCL10_(1–73) without exerting cellular toxicity. HMVEC chemotaxis was measured towards A 30 ng/ml FGF-2 and B EBM-2 \(+\) 0.4% FCS treated cells (CO) in the presence or absence of CXCL10_(1–77) or CXCL10_(1–73). The data are displayed as median (± IQR) of 4 to 7 independent experiments. Statistically significant differences in migration compared to cells treated with control medium or FGF-2 were determined by a Mann–Whitney U test (** p ≤ 0.01, *** p ≤ 0.001 for comparison to control, $$ p ≤ 0.01 for comparison to FGF-2). C FGF-2-induced proliferation of HMVEC was examined in the presence or absence of CXCL10_(1–77) or CXCL10_(1–73). The data are displayed as mean (± SEM) of 5 to 7 independent experiments. Statistically significant differences in proliferation compared to cells treated with 10 ng/ml FGF-2 were determined by an unpaired t-test ($ p ≤ 0.05; $$ p ≤ 0.01). D Cellular toxicity was assessed after 30 h of stimulation with CXCL10_(1–77) or CXCL10_(1–73). The median (± IQR) of 3 to 4 independent experiments is shown. Statistically significant differences in cell viability compared to cells treated with control were determined by a Mann–Whitney U test (*** p ≤ 0.001). E Representative images are displayed of HMVEC treated with control medium (CO; MCDB131 + 0.4% [v/v] FCS), 2% (v/v) Triton X-100 to induce cell death, and 360 nM of CXCL10_(1–77) or CXCL10_(1–73). Scale bar = 400 µm