Fig. 2.

IP-10 induces in vivo vessel regression. (A) Wound biopsies from wild-type (WT) and CXCR3^–/– (CXCR3 KO) mice were immunostained for vWF. In unwounded tissue, very few vessels are observed in either the WT or CXCR3 KO mice. Following wounding there is a greater number of vessels observed in the CXCR3 KO mice at day 14 and 30 compared to WT. Scale bar: 250 μm. (B) Quantitative analysis of the number of vessels in A. The CXCR3 KO mice at day 14 have a twofold increase and at day 30 have a threefold increase in vessels compared to WT. Solid bars, WT mice; hatched bars, CXCR3 KO. Values are mean ± s.e.m. This suggests that CXCR3 plays a role in regulating vascular regression during the wound-healing process. (C) VEGF-A (150 ng/ml) supplemented GFR-Matrigel was injected into the groin of mice. After 10 days the Matrigel was removed (control, n=3) to show vessel invasion (10 days). For the remaining mice (n=10), one side was injected with mIP-10 (5 μg) at days 10 and 12. The other side was treated with an equal volume of saline (diluent). At day 17, the Matrigel was removed and stained with Masson's trichrome to identify vessels. Treatment with IP-10 (17 day IP-10) shows a significant regression of vessels compared to saline control (17 day saline). These data indicated that IP-10 is able to directly cause vessel regression. Representative data are shown; n=3. Scale bar: 500 μm.