title: Proteomics of post-traumatic proliferative vitreoretinopathy in rabbit retina reveals alterations to a variety of functional proteins.
abstract: OBJECTIVE
  The purpose of this study was to investigate the protein profiles and pathogenesis in rabbit retinas from normal and post-traumatic proliferative vitreoretinopathy (PVR).
  
  
  METHODS
  A modified rabbit model of post-traumatic PVR was modified used in the study. Two-dimensional gel electrophoresis (2-DE) coupled with mass spectrometry (MS) were utilized to identify the changes to the protein profiles of rabbit retina. The myosin light chains-2 (MLC2) was subsequently chosen as a target for its biggest difference in 2-DE gels using Western blot, immunohistochemistry and MTT assay.
  
  
  RESULTS
  Comparative gel analysis revealed that 20 spots were up-regulated or novel emerged and 12 were down-regulated or even disappeared in PVR retinas. The majority of changes could consist of the following functional groups of proteins including the cell skeleton proteins; the wound healing/cell adhesion proteins; the proteins involved in metabolism and in blood-retina barrier destruction; oxidative stress-related proteins and the ion channel proteins. Western blot analysis confirmed that MLC2 protein expression was upregulated in PVR retinas. MTT assay showed that the anti-MLC2 monoclonal antibody significantly decreased the proliferation in ARPE-19 cells stimulated with different concentrations and times in vitro experiment.
  
  
  CONCLUSIONS
  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. The data reported may be useful for further studies on pathogenesis of human PVR and for the screening of biomarkers to develop new potential therapeutic approaches.
authors.affiliation: The First Affiliated Hospital of Chongqing Medical University, Chongqing Key Laboratory of Ophthalmology, Chongqing, PR China.
authors.forename: Qingyun
authors.initials: Q
authors.lastname: Zhou
authors.forename: Guangjun
authors.initials: G
authors.lastname: Xu
authors.forename: Xuedong
authors.initials: X
authors.lastname: Zhang
authors.forename: Chen
authors.initials: C
authors.lastname: Cao
authors.forename: Zhongqiang
authors.initials: Z
authors.lastname: Zhou
mesh_terms: D000818:Animals; D001813:Blood-Retinal Barrier / Q000502:physiology; D015153:Blotting, Western; D002478:Cells, Cultured; D004195:Disease Models, Animal; D005131:Eye Injuries / Q000150:complications* / Q000378:metabolism / Q000473:pathology; D005136:Eye Proteins / Q000378:metabolism*; D005260:Female; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D013058:Mass Spectrometry; D018384:Oxidative Stress; D020543:Proteome / Q000378:metabolism*; D040901:Proteomics / Q000379:methods*; D011817:Rabbits; D055213:Retinal Pigment Epithelium / Q000378:metabolism* / Q000473:pathology; D018630:Vitreoretinopathy, Proliferative / Q000209:etiology / Q000378:metabolism* / Q000473:pathology
chemical_list: D005136:Eye Proteins; D020543:Proteome