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Background <p>This study aims to investigate the role of inflammation in proliferative vitreoretinopathy (PVR) by analysing inflammation-related proteins in vitreous samples and identifying potential biomarkers for PVR severity.</p> Methods <p>Vitreous samples were collected from patients with different stages of PVR (control group, <i>n</i> = 15; PVR A/B, <i>n</i> = 15; PVR C/D, <i>n</i> = 14). Using an Onlink proteomics panel, the levels of 92 inflammation-related proteins were measured. Differential expression analysis was conducted to identify proteins significantly altered between the PVR and control groups. AlphaFold3 modelling was employed to predict common binding peptide segments among differentially expressed proteins. Additionally, the impact of PVR vitreous on inflammatory cytokine production in retinal pigment epithelium (RPE) cells was assessed to explore the functional consequences of the observed protein changes.</p> Results <p>The proteomic analysis revealed differential expression of 63 inflammation-related proteins between the PVR and control groups. Among these, MCP-1 exhibited significant variations across PVR stages and demonstrated high diagnostic value for PVR presence (AUC = 0.949) and severity (PVR C/D, AUC = 0.719). AlphaFold3 modelling identified a common binding peptide segment, INAPVTCCYN, shared by MCP-1, CCL3, CCL4 and CXCL9, suggesting their potential collaborative role in PVR progression. Furthermore, vitreous samples from PVR patients significantly stimulated inflammatory cytokine production in RPE cells, indicating a functional link between vitreous inflammation and retinal pathology.</p> Conclusions <p>PVR is associated with elevated levels of vitreous inflammation and MCP-1 is a promising biomarker for predicting and diagnosing PVR severity. The identification of a common binding peptide segment and the stimulation of cytokine production in RPE provide mechanistic insights into PVR progression.</p>

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Olink proteomics profiling platform reveals inflammatory protein biomarkers in vitreous with different degrees of proliferative vitreoretinopathy

  • 期刊论文

  • 发表日期：

    2026年3月9日

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  • Xiaohuan Zhao,
  • Siyang Han,
  • Huiyi Jin,
  • Hong Wang,
  • Xiaolu Yang,
  • Xiaodong Sun

摘要

Background

This study aims to investigate the role of inflammation in proliferative vitreoretinopathy (PVR) by analysing inflammation-related proteins in vitreous samples and identifying potential biomarkers for PVR severity.

Methods

Vitreous samples were collected from patients with different stages of PVR (control group, n = 15; PVR A/B, n = 15; PVR C/D, n = 14). Using an Onlink proteomics panel, the levels of 92 inflammation-related proteins were measured. Differential expression analysis was conducted to identify proteins significantly altered between the PVR and control groups. AlphaFold3 modelling was employed to predict common binding peptide segments among differentially expressed proteins. Additionally, the impact of PVR vitreous on inflammatory cytokine production in retinal pigment epithelium (RPE) cells was assessed to explore the functional consequences of the observed protein changes.

Results

The proteomic analysis revealed differential expression of 63 inflammation-related proteins between the PVR and control groups. Among these, MCP-1 exhibited significant variations across PVR stages and demonstrated high diagnostic value for PVR presence (AUC = 0.949) and severity (PVR C/D, AUC = 0.719). AlphaFold3 modelling identified a common binding peptide segment, INAPVTCCYN, shared by MCP-1, CCL3, CCL4 and CXCL9, suggesting their potential collaborative role in PVR progression. Furthermore, vitreous samples from PVR patients significantly stimulated inflammatory cytokine production in RPE cells, indicating a functional link between vitreous inflammation and retinal pathology.

Conclusions

PVR is associated with elevated levels of vitreous inflammation and MCP-1 is a promising biomarker for predicting and diagnosing PVR severity. The identification of a common binding peptide segment and the stimulation of cytokine production in RPE provide mechanistic insights into PVR progression.