Vascular endothelial growth factor (VEGF) is regulated under hypoxic conditions and promotes angiogenesis. We investigated the expression pattern of VEGF and its regulation by somatostatin (SRIF) in the mouse retina under normal conditions and in the presence of an ischemic state, characterized by marked hypoxia.

We showed that in normal retinas VEGF immunoreactivity is abundantly expressed in a variety of neuronal elements (cone photoreceptors, multiple populations of bipolar cells, and ganglion cells) and scarcely in retinal vessels. In ischemic conditions, a dramatic increase of VEGF was observed in retinal vessels, whereas it almost disappeared from retinal neurons. In addition, VEGF release increased significantly, and this response was contrasted by SRIF or octreotide, a SRIF subtype receptor 2 (sst2) preferring agonist. In line with these results, VEGF expressed by retinal vessels in response to the ischemic status was significantly reduced in sst1 knock-out retinas, which are characterized by over-expression and constitutive activation of sst2, and in wild-type retinas treated with SRIF or octreotide.

Together, these data suggest that VEGF expression pattern and release is subjected to profound changes in the presence of an ischemic state. VEGF remodelling in retinal blood vessels may follow the onset of proliferating retinal pathologies and SRIF, likely acting at sst2, may provide an important regulation of these changes.