Background  Proliferative vitreoretinopathy (PVR) is one typically possible complication of ocular trauma with the reactive process of the ocular tissue resulting in growth and contraction of proliferative membranes within the vitreous cavity and the surface of the retina. It’s the multiple-factor mediated wound-healing process with ambiguous pathogenesis and inefficient drug therapy.
Methods  A modified rabbit model of post-traumatic PVR was used to investigate the mechanism of different stages. Two-dimensional gel electrophoresis (2-DE) and mass spectrometry (MS) were utilized to identify the changes to the protein profiles in whole retina of rabbit in early period (day 15) of PVR, advanced stage (day 60) of PVR and normal controls. In addition, western blot was subsequently performed to validate the results of 2-DE and MS on a significantly increased expression protein using retina samples from these three groups.
Results  In the current research, the proliferative effect of treatment at early period (day 15) was not severe which could be described as grade A PVR, at advanced stage(day 60) was significant which could be described as grade B or grade C PVR according to the updated Retina Society Classification (1991). Above 1000 protein spots were visible on the different range gels with abundant proteins detected at the 30-75 kDa range as well as the pH between 5-7. Comparative gel analysis revealed 32 protein spot differently expressed (>1.5-fold difference in visible abundance) in rabbit retinas undergoing ocular traumatic operation. Twelve of the 32 spots were decreased or even disappeared, whereas 20 spots were increased or novel emerged. The majority of changes could consist of the following functional groups of proteins including the cell skeleton proteins, distinguished myosin light chains-2 and troponin; the wound healing/cell adhesion proteins, such as arginase and kininogen; the proteins involved in metabolism and in blood-retina barrier destruction, for instance, the carbonic anhydrase II and complement components; oxidative stress-related proteins, notably alpha A-crystallin; and the ion channel proteins.
Conclusion  Our results suggested that PVR is a complicated pathology process with alterations in expression of a variety of functional proteins rather than a single key protein.