Background: Diabetic Retinopathy (DR), one of the major microvascular complications
commonly occurring in diabetic patients, can be classified into Proliferative Diabetic Retinopathy
(PDR) and Non-Proliferative Diabetic Retinopathy (NPDR). Currently, available therapies are only
targeted for later stages of the disease in which some pathologic changes may be irreversible. Thus,
there is a need to develop new treatment options for earlier stages of DR through revealing pathological
mechanisms of PDR and NPDR.
Objective: The purpose of this study was to characterize the proteomes of diabetes through quantitative
analysis of PDR and NPDR.
Methods: Vitreous body was collected from three groups: control (non-diabetes mellitus), NPDR,
and PDR. Vitreous proteins were digested to peptide mixtures and analyzed using LC-MS/MS.
MaxQuant was used to search against the database and statistical analyses were performed using
Perseus. Gene ontology analysis, related-disease identification, and protein-protein interaction
were performed using the differential expressed proteins.
Results: Twenty proteins were identified as critical in PDR and NPDR. The NPDR group showed
different expressions of kininogen-1, serotransferrin, ribonuclease pancreatic, osteopontin, keratin
type II cytoskeletal 2 epidermal, and transthyretin. Also, prothrombin, signal transducer and activator
of transcription 4, hemoglobin subunit alpha, beta, and delta were particularly up-regulated proteins
for PDR group. The up-regulated proteins related to complement and coagulate cascades.
Statherin was down-regulated in PDR and NPDR compared with the control group. Transthyretin
was the unique protein that increased its abundance in NPDR compared with the PDR and control
Conclusion: This study confirmed the different expressions of some proteins in PDR and NPDR.
Additionally, we revealed uniquely expressed proteins of PDR and NPDR, which would be differential
biomarkers: prothrombin, alpha-2-HS-glycoprotein, hemoglobin subunit alpha, beta, and transthyretin.