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Wound-induced angiogenesis and its pharmacologic inhibition in a murine model
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.
Insights
The novel compound SU5416 effectively inhibits wound-induced angiogenesis in mice during treatment. However, this anti-angiogenesis effect is temporary, with angiogenesis fully recovering after SU5416 treatment stops.
Area of Science:
- Biomedical research
- Pharmacology
- Angiogenesis research
Background:
- SU5416 is a novel synthetic compound known to inhibit tumor growth.
- Angiogenesis, the formation of new blood vessels, is crucial for both tumor development and wound healing.
- This study investigates the potential of SU5416 to inhibit angiogenesis in the context of wound healing.
Purpose of the Study:
- To determine if SU5416 inhibits angiogenesis induced by wound healing.
- To evaluate the effect of SU5416 on microvessel density in a murine wound model.
Main Methods:
- Sixteen female BALB/c mice were used, divided into two groups: SU5416 treatment (n=8) and vehicle control (n=8).
- Mice received SU5416 or vehicle starting two days before wound chamber implantation and treatment ceased on day 7.
- Microvessel density was assessed using micrographs taken on days 1, 7, and 14 post-implantation.
Main Results:
- No significant difference in microvessel density was observed on day 1.
- SU5416 significantly inhibited angiogenesis by day 7 (P <.001).
- Angiogenesis fully recovered seven days after treatment cessation, with no significant difference from controls on day 14.
Conclusions:
- SU5416 inhibits wound-induced angiogenesis in a murine model, similar to its effect on tumor-induced angiogenesis.
- The anti-angiogenic effect of SU5416 is significant only during the period of active treatment.
- Wound healing angiogenesis is reversible upon discontinuation of SU5416 therapy.