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Targeting of junctional adhesion molecule-C inhibits experimental choroidal neovascularization

Xu Hou1, Dan Hu, Yu-sheng Wang

  • 1Department of Ophthalmology, Eye Institute of Chinese PLA, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.

Investigative Ophthalmology & Visual Science
|February 11, 2012
PubMed
Abstract

Insights

Targeting junctional adhesion molecule-C (JAM-C) suppressed choroidal neovascularization (CNV) by inhibiting macrophage and retinal pigment epithelial cell migration and RPE barrier dysfunction. This suggests JAM-C blockade is a potential therapeutic strategy for CNV.

Area of Science:

  • Ophthalmology
  • Cell Biology
  • Immunology

Background:

  • Choroidal neovascularization (CNV) is a major cause of vision loss.
  • Junctional adhesion molecule-C (JAM-C) is implicated in inflammatory processes and cell migration.

Purpose of the Study:

  • To investigate JAM-C expression in CNV.
  • To evaluate the therapeutic potential of targeting JAM-C in CNV formation and related cellular functions.

Main Methods:

  • JAM-C expression was analyzed using RT-PCR, immunoblotting, and immunofluorescence.
  • CNV, vascular leakage, and macrophage infiltration were quantified in vivo.
  • Macrophage transmigration, RPE cell migration, and RPE permeability were assessed in vitro.

Main Results:

  • JAM-C expression was significantly upregulated in CNV.
  • Targeting JAM-C with an Fc chimera inhibited CNV, leakage, and macrophage infiltration.
  • JAM-C knockdown reduced RPE cell migration and monolayer permeability.

Conclusions:

  • JAM-C plays a critical role in CNV pathogenesis.
  • Blocking JAM-C demonstrates therapeutic potential for treating CNV.
  • JAM-C inhibition may be a viable strategy for suppressing CNV by targeting key cellular processes.

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