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Editors Selection IGR 7-1

Basic Science: Proteomics

Comment by Gülgün Tezel on:

51709 Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells, Bell K; Funke S; Pfeiffer N et al., PLoS ONE, 2012; 7: e46910

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Serum and antibodies of glaucoma patients lead to changes in the proteome, especially cell regulatory proteins, in retinal cells Bell K, Funke S, Pfeiffer N, Grus FH PLoS ONE 2012; 7: e46910 In this study, Bell et al. aimed to determine whether the serum of patients with glaucoma or the isolated serum antibodies interact with neuroretinal proteins in cell cultures. The authors detected significant changes in protein expression following incubation of R28 and RGC5 cell lines with the glaucomatous serum. They suggested that the serum antibodies change the expression of proteins involved in regulatory cellular processes and thereby increase the neuronal susceptibility to apoptosis in glaucoma.

The inspiring work and continuing efforts of the authors to illuminate the autoimmune mechanisms of glaucomatous neurodegeneration are well appreciated; however, the results of this study should be viewed more conservatively for a number of reasons. Firstly, the studied cell lines may not properly represent retinal ganglion cells, or the in–vitro system may be limited in modeling the elevated intraocular pressure in human glaucoma. Protein expression changes also need further validation. In addition, the authors should consider the possibility that many factors present in the studied model, such as serum components activating the complement, cross-reactive serum proteins initiating a receptor-mediated signaling, or endocytosed serum molecules inducing intracellular housecleaning processes, might possibly result in protein expression changes in cultured cells, which may not necessarily be relevant to apoptotic processes. The lack of any change in cell survival after serum incubations also questions a causal relationship.

Previous ex-vivo evidence supports that antibodies at concentrations similar to those detected in the glaucomatous patient serum can be internalized by retinal neurons and increase the susceptibility for neuronal injury in the isolated human retina.¹ However, recent in-vivo studies of Rag1-/- mice lacking T and B lymphocytes have produced conflicting observations, supportive or unsupportive of autoantibodymediated neuronal injury^2,3 depending on the experimental model to induce ocular hypertension, follow-up time, extent of neuronal injury, and assessment techniques. Further work testing the importance of autoantibodies for glaucomatous neurodegeneration in relevant models would be highly interesting.

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