Abstract
Proliferative vitreoretinopathy (PVR) develops as a complication of retinal detachment surgery and represents a devastating condition leading to serious vision loss. A good animal model that permits extensive functional studies and drug testing is crucial in finding better therapeutic modalities for PVR. A previously established mouse model, using dispase injection, was analyzed from the proteomic point of view, examining global protein profile changes by 2D electrophoresis, image analysis and HPLC–tandem mass spectrometry‐based protein identification. The easy applicability of the mouse model was used to study the role of transglutaminase 2 (TG2) in PVR formation by proteomic examination of dispase‐induced TG2 knockout vitreous samples. Our data demonstrate that, despite the altered appearance of crystallin proteins, the lack of TG2 did not prevent the development of PVR.
Highlights
Proliferative vitreoretinopathy (PVR) develops as a complication of retinal detachment surgery and represents a devastating condition leading to serious vision loss
The WT Ctrl group was created from the three gel images originating from physiological saline-treated samples and the WT PVR group was created from the three gel images originating from dispase-treated samples
That transglutaminase 2 (TG2) may affect the timing of PVR formation but we do not have such information as we examined the already formed PVR condition only
Summary
Proliferative vitreoretinopathy (PVR) develops as a complication of retinal detachment surgery and represents a devastating condition leading to serious vision loss. A good animal model that permits extensive functional studies and drug testing is crucial in finding better therapeutic modalities for PVR. In PVR formation by proteomic examination of dispase-induced TG2 knockout vitreous samples. Proliferative vitreoretinopathy (PVR) develops as a complication in 8–25% of patients undergoing primary retinal detachment surgery. It is a multifactorial disease induced by a variety of factors [1]. We have shown activation of neural progenitor cells in human eyes with PVR near the pars plana region, from which only the glial population seemed to respond to retinal injury by targeted migration into the vitreous [4]
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Free) 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a call
