Ocular neovascularization

The molecular cascade leading to neovascularization is complex and can vary in different tissues and different disease processes. Each tissue has its own unique microenvironment with potential differences in blood vessels, surrounding cells, and extracellular matrix. These differences can result in differences in constitutive and induced-expression of neovascularization-related proteins or they can alter the effects of proteins; some proteins promote neovascularization in one setting and inhibit it in others. Proteins depend upon other molecules for their actions, and lack of expression of a binding partner in a tissue can have a major impact on the effect of a protein in that setting. In order to define the potential actions of a protein and its interactions with other proteins in neovascularization, it is useful to study its effects in several well-characterized vascular beds and different pathologic processes. The eye is an important organ in which to study neovascularization, because it has several useful features that facilitate such study, and also because neovascular diseases are prevalent causes of visual morbidity and blindness. The eye contains several vascular beds separated by avascular tissue. The vascular beds can be visualized in vivo, and the presence of neovascularization can be unequivocally identified and quantified because of the surrounding avascular tissue. Also, retina-specific promoters combined with inducible promoter systems provide a useful way to control expression of proteins of interest. By observing the different effects of proteins in different vascular beds in the eye, at different stages of development, and in different disease models, a more complete picture of the protein's actions and interactions with other proteins can emerge.