Expression of wild-type p53-induced phosphatase 1 in diabetic epiretinal membranes.

Jiping Xu,Qianqian Lan,Li Li,Min Li,Hui Huang,Ling Cui,Xin Zhao,Li Jiang,Yu Wu,Wenjing He,Siming Zeng,Haibin Zhong,Fan Xu,Lifei Chen

doi:10.18632/oncotarget.16683

Abstract

ObjectiveThe aims of the present study were to investigate the expression and distribution of Wild-type p53-induced phosphatase 1 (Wip1) in diabetic patients with proliferative diabetic retinopathy (PDR) with epiretinal membranes (ERMs) meanwhile analyze the colocalization of Wip1 and nuclear factor kappa-B (NF-κB) p65 in ERMs.MethodsERMs samples were collected from patients with PDR (PDR group) or non-diabetic patients with idiopathic epiretinal membranes (iERMs) (control group) during pars plana vitrectomy. Real-Time PCR analysis was carried out to examine the mRNA expression of Wip1 in ERMs. Immunohistochemical analysis and Immunofluorescent analysis were performed to detect the protein expression of Wip1 in ERMs. Double immunofluorescent staining was performed to detect the colocalization of Wip1 and glial fibrillary acidic protein (GFAP) (retinal glial cells marker), also Wip1 and NF-κB.ResultsERMs were obtained from 17 eyes of 17 patients with PDR (the PDR group) and 9 eyes of 9 nondiabetic patients (the control group) with iERMs. Our results showed high expression levels of Wip1 mRNAs in ERMs after PDR, but low in iERMs. In addition, both immunohistochemistry and immunofluorescence assay showed strong immunoreactivity for Wip1 in PDR ERMs. Furthermore, Wip1 and GFAP were coexpressed in PDR membranes. Finally, the expression of Wip1 was paralleled with NF-κB.ConclusionThese data support the notion that Wip1 contributes to the formation of the ERMs in PDR membranes via NF-κB signaling.

Highlights

Diabetic retinopathy (DR) is one of the leading causes of decreased vision and blindness in the workingage population of developed countries [1, 2]
These data support the notion that Wild-type p53-induced phosphatase 1 (Wip1) contributes to the formation of the epiretinal membranes (ERMs) in Proliferative diabetic retinopathy (PDR) membranes via NF-κB signaling
ERMs were obtained from 17 eyes of 17 patients with PDR and 9 eyes of 9 nondiabetic patients with idiopathic epiretinal membranes

Summary

Introduction

Diabetic retinopathy (DR) is one of the leading causes of decreased vision and blindness in the workingage population of developed countries [1, 2]. Proliferative diabetic retinopathy (PDR) is the more advanced form of DR, characterized by outgrowth of epiretinal membranes at the vitreoretinal interface [3]. These epiretinal membranes (ERMs) may cause distortion of the retinal architecture, vascular leakage, secondary retinal edema and rhegmatogenous retinal detachment [4]. Glial cell proliferation following PDR is suggested to play a crucial role in ERMs formation [4,5,6]. Glial cell proliferation involves a complex cross-talk among retinal glial cells, including Müller cells and astrocytes [5, 6]. The exact mechanisms that regulate the formation of epiretinal membranes in PDR are still incompletely understood

Methods

Results

Conclusion