Wound-induced angiogenesis and its pharmacologic inhibition in a murine model

Abstract

Background. A novel synthetic compound, SU5416, inhibits subcutaneous tumor growth of cells. Because angiogenesis in tumor growth and wound healing involves similar mechanisms, we examined whether SU5416 inhibits wound-induced angiogenesis. Methods. Sixteen female BALB/c mice were randomized to receive either SU5416 (n = 8) or vehicle alone (n = 8) on day -2. On day 0, transparent window chambers were implanted into the dorsal skin flap. Treatment was stopped on day 7. On days 1, 7, and 14, micrographs of the windows were taken and microvessel density was estimated. Results. On day 1, no statistically significant difference was noted between the microvessel density in controls and treatments. After the mice underwent treatment from day -2 to day 7 and microvessel densities were analyzed on day 7, angiogenesis was significantly inhibited in the SU5416 group (P < .001). Seven days after cessation of treatment, however, the SU5416 group showed complete recovery in angiogenesis. The increase in microvessel density in the SU5416 group on day 14 from day 7 was not significantly different from that of the control group (P > .05). Conclusions. We observed that SU5416, a known inhibitor of tumor-induced angiogenesis, also inhibited wound-induced angiogenesis in our murine wound model. This inhibitory effect is significant while the mice are undergoing treatment.