Abnormal maturation of the retinal vasculature in type XVIII collagen/endostatin deficient mice and changes in retinal glial cells due to lack of collagen types XV and XVIII

SPECIFIC AIMSLack of collagen XVIII, containing the antiangiogenic endostatin-fragment, results in delayed regression of the hyaloid vessels and poor outgrowth of the retinal vessels. This study was originated to assess the roles of the homologous collagens XV and XVIII in the development of eye vasculature. Mice lacking both collagens XV and XVIII were studied to gain insight on their distinct and possible compensatory functions.PRINCIPAL FINDINGS1. Lack of type XVIII collagen induces an increased number of astrocytes in the retinaAstrocytes are known to form a template for growing vessels in the retina. However, the poor outgrowth of retinal vessels in type XVIII collagen null mice was not associated with defective proliferation and migration of astrocytes. Instead, retinal whole mounts on postnatal day 10 revealed an increase in the amount of astrocytes.2. The retina in Col18a1−/− mice is vascularized by anomalous anastomoses from a persistent fetal vasculature in the vitreous bodyThe retinal angiogene...