Ocular trauma and surgery are considered the most common cause for proliferative vitreoretinopathy (PVR). Many retinal cell types are thought to be the cellular source for PVR although most risk factors for PVR are associated with intravitreal dispersion of the retinal pigment epithelium (RPE) cells. Major PVR animal models are rabbit and swine with an artificial implantation of exogenous cells into the vitreous to form epiretinal membrane (ERM) which does not recapitulate a real PVR pathology. To clarify and validate the participation of RPE cells, to mimic ocular trauma in situ, and to reveal the related macromolecule changes in PVR pathology, we utilized a dispase treatment to damage the retina in establishment of a reliable RPE-tagged PVR mouse model with ERM-like tissues formed within and on both surface of the retina. The immunostaining of patient epiretinal membranes with lineage markers confirms RPE is involved in PVR development. Quantitative PCR analysis indicates the dedifferentiation of RPE cells switches RPE from epithelial to mesenchymal phenotype to re-enter a proliferative and mobile state underlying PVR. Gene expression results of the mouse PVR model retinas are consistent with the microarray gene expression profile of human PVR retinas, validating that our mouse PVR model resembles human PVR and is thereby suitable for molecular mechanism and pharmaceutical studies.

The purpose of this study was to evaluate the impact of vitrectomy and posterior hyaloid (PH) peeling on color alteration of optic nerve head (ONH) and retina as a surrogate biomarker of induced perfusion changes.

Short chain fatty acids (SCFAs) produced by gut microbiota are known to play primary roles in gut homeostasis by immunomodulation partially through G-protein coupled receptors (GPR) 43. Using mouse models of TLR ligand induced keratitis, we investigated whether SCFAs and GPR43 play any regulatory roles in the pathogenesis of inflammatory responses in the eye.

Autoimmune diseases caused by T cells can arise from either T-helper 1 (Th1) or T-helper 17 (Th17)-type pathogenic T cells. However, it is unclear whether these two T-cell subsets are influenced by distinct pathogenic factors and whether treatments that are effective for Th1 responses also work for Th17 responses. To compare these two pathogenic responses, we conducted a systematic analysis in a mouse model of experimental autoimmune uveitis (EAU) to identify the factors that promote or inhibit each response and to determine their responses to various treatments. Our study found that the two types of pathogenic responses differ significantly in their pathological progressions and susceptibility to treatments. Specifically, we observed that extracellular adenosine is a crucial pathogenic molecule involved in the pathogenicity of inflammation and T-cell reactivity and that reciprocal interaction between adenosine and gamma delta (γδ) T cells plays a significant role in amplifying Th17 responses in the development of autoimmune diseases. The potential effect of targeting adenosine or adenosine receptors is analyzed regarding whether such targeting constitutes an effective approach to modulating both γδ T-cell responses and the pathogenic Th17 responses in autoimmune diseases.