The role of microRNA24 in ocular fibrosis
Description
The topic for this thesis is the role of microRNA24 in ocular fibrosis, with an emphasis on this small biomolecule's potential to minimize a fibrotic response in ocular pathologies. This thesis investigates the hypothesis that microRNA24 is capable of preventing endothelial to mesenchymal cell transition (EndoMT) as well as epithelial to mesenchymal transition (EMT) to thus minimize subretinal fibrotic scarring and associated damage in retinal pathologies such as age-related macular degeneration. Furthermore, this investigation seeks to further elucidate the mechanisms by which microRNA24 may act to minimize or prevent fibrosis. Chapter 1 discusses the rationale for this investigation, detailing the role and mechanisms of ocular fibrosis, particularly in retinal pathologies, and reviewing the established effects of microRNA24. Additionally, Chapter 1 addresses the therapeutic relevance of this research and focuses the research goals into explicit aims. Chapter 2 presents results from in vitro experiments which suggest microRNA24 has the potential to prevent EMT of retinal pigment epithelium cells, while Chapter 3 discusses experimental data which may indicate that microRNA24 can also prevent EndoMT of endothelial cells. Chapter 4 assesses the contributions of the thesis to the field, evaluates completion of research aims, and suggests further experiments. This thesis presents novel findings that suggest microRNA24 may have the potential to prevent both EMT and EndoMT, which could ameliorate ocular fibrosis and have significant therapeutic impact.