UC San Diego

Wound healing is paramount for the survival of multicellular organisms, but this process can lead to scarring if left uncontrolled. Retinal scarring, in particular, occurs in many prevalent retinal diseases and can be devastating as this pathology leads to blindness. Unfortunately, little is known about retinal scarring, such as the origin of cells producing the scar and the cellular mechanisms leading to scar formation. Understanding these elements behind scar production is vital in creating therapeutic targets that can prevent potential blindness in those affected by retinal scarring. Although there are many retinal disease models in mice, a reliable mouse retinal scarring model has not been established. In this study, I develop two scarring models in mice. One is a mouse model for the disease phthisis bulbi, which is characterized as a shrunken, non-functional eye that is caused by injury, inflammation or other infections. We induce these characteristic symptoms by injecting dispase, a neutral protease, into the eyes of mice, causing degradation of retinal tissue, eye shrinkage, and the production of scars. The other scarring model is termed as Long Oxygen Induced Retinopathy (LOIR), which is a more pathologically severe model of the traditional “Smith” OIR mouse model of retinopathy of prematurity. This newly developed scar producing model is induced by prolonging the exposure of highly concentrated atmospheric oxygen from the traditional “Smith” OIR model protocol of 5 days to 14 days. With these models, I answer what cell type(s) are producing scar tissue in the retina.