Vitreous cytokines and regression of the fetal hyaloid vasculature

Abstract

The fetal hyaloid vasculature plays a critical role in many aspects of proper ocular development. The hyaloid artery (HA) is a large vessel that extends from the optic disc through the vitreous where it branches and extends to the posterior surface of the lens to anastamose with the tunica vasculosa lentis (TVL) which supplies nutrients to the developing lens in the fetus (Figure I.D-1). In humans, the entire embryonic vascular system regresses by birth, which is necessary for media clarity and normal vision. Regression of the hyaloid vasculature is a very complex process likely requiring the participation of many proteins. The mechanisms of hyaloid vessel regression are not known, but insight could be obtained by understanding how this fetal vasculature forms. One study of human embryonic vitreous revealed the presence of blood islands composed of aggregates of primitive erythroblasts and hemangioblasts, as early as the seventh week of gestation (WG) [1]. These cell aggregates express hematopoietic stem cell markers, and the ligands for these markers are expressed in high concentrations in the lens and retina, probably functioning to guide the cells into the vitreous body assembling the fetal vitreous vasculature by hemo-vasculogenesis [2].