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Fig. 5 | Cell Communication and Signaling

Fig. 5

From: Natural carboxyterminal truncation of human CXCL10 attenuates glycosaminoglycan binding, CXCR3A signaling and lymphocyte chemotaxis, while retaining angiostatic activity

Fig. 5

Equivalent inhibition of spontaneous HMVEC migration and invasion by intact CXCL10(1–77) or C-terminally truncated CXCL10(1–73). After creating a scratch wound, spontaneous HMVEC migration and invasion was monitored for 17 h in EBM-2 \(+\) 1% FCS (CO) in the presence or absence of CXCL10(1–77) or CXCL10(1–73) using the IncuCyte S3 Live-Cell Analysis System. Percentages of A relative wound density and B wound confluence compared to medium-treated cells were represented in bar plots. The data are displayed as mean (± SEM) of 4 to 7 independent experiments. Unpaired t-test was used to compare differences in relative wound density and wound confluence compared to EBM-2 \(+\) 1% FCS treated cells (CO) (* p ≤ 0.05, ** p ≤ 0.01, *** p ≤ 0.001). C Representative images of the wound borders using immunofluorescence microscopy after calcein staining of HMVEC stimulated with EBM-2 \(+\) 1% FCS (CO), CXCL10(1–77) or CXCL10(1–73) at 120 nM. Scale bar = 100 µm. D Representative images of the full wound area using IncuCyte time-lapsed microscopy pictures of HMVEC stimulated with EBM-2 \(+\) 1% FCS (CO), CXCL10(1–77) or CXCL10(1–73) at 12 nM and 120 nM. Scale bar = 400 µm

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