![]() Levels of VEGF released into the medium, as determined by ELISA, were approximately twofold higher after MMP-9 treatment and could be blocked by GM6001. This could be blocked by the MMP-inhibitor, GM6001. In vitrotreatment of normal islets cocultured with endothelial cells with MMP-9, but not MMP-2, trypsin, urokinase or collagenase P, resulted in an angiogenic phenotype. ![]() There was an upregulation of both MMP-2 and MMP-9 in association with the angiogenic switch. Angiogenic islets cocultured with endothelial cells showed endothelial sprouting: this was not observed in nonangiogenic islets and furthermore could be blocked by a VEGF neutralising antibody, supporting a role for VEGF in the angiogenic process. ![]() Immunohistochemical analysis showed universal expression of VEGF and its receptors, although the VEGF-VEGF-R2 complex was only detected in angiogenic islets and in tumours. Treatment with the SU5416 prevented activation of the angiogenic switch in 94% of hyperplastic islets and reduced tumour growth by 75%.
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