In acute injury of retina such as retinal detachment or ocular trauma, proliferative vitreoretinopathy (PVR), an excessive retinal gliosis in complex with inflammatory, excessive wound healing and remodeling processes, is a major barrier of surgical repair, leading to blindness despite the tremendous technological advancement in retinal surgery. The complex process of PVR formation has not been completely understood until now and currently there is no subsiding or complete treatment available.
Müller cells respond rapidly to all pathologic stress of retinal tissue, characterized by initial increased expression of intermediate filament (IF) proteins such as glial fibrillary acidic protein (GFAP). In certain conditions, such as retinal detachment or ocular trauma, this response further progresses into proliferative stages of Müller cells. The molecular mechanisms that control context-dependent behavior of Müller cells are unclear. My specific questions in this regard are: (1) What is the functional significance of activated intermediate filament of Müller cells in PVR formation?; (2) What triggers Müller cell entry into the proliferative stage that results in PVR formation?; (3) How do activated Müller cells affect consequential or combined processes such as epithelial mesenchymal transition (EMT) and inflammatory processes in PVR?