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A Mouse Model for Laser-induced Choroidal Neovascularization
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Choroidal Neovascularization Is Inhibited in Splenic-Denervated or Splenectomized Mice with a Concomitant Decrease in

Xue Tan1, Katsuhito Fujiu2,3,4, Ichiro Manabe5

  • 1Department of Ophthalmology, Graduate School of Medicine and Faculty of Medicine, The University of Tokyo, Tokyo, Japan.

Plos One
|August 18, 2016
PubMed
Summary
This summary is machine-generated.

Sympathetic activity, particularly through Ly6Chi macrophages, exacerbates choroidal neovascularization (CNV) in mice. Targeting this pathway may offer new therapeutic strategies for CNV.

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Area of Science:

  • Ophthalmology
  • Immunology
  • Neuroscience

Background:

  • Choroidal neovascularization (CNV) is a major cause of vision loss.
  • The role of the sympathetic nervous system in CNV pathogenesis is not fully understood.

Purpose of the Study:

  • To investigate the involvement of sympathetic activity in CNV development using a laser-induced mouse model.
  • To identify specific immune cell populations mediating CNV.

Main Methods:

  • Laser-induced CNV model in mice.
  • Flow cytometry to analyze intraocular immune cells (lymphocytes, granulocytes, macrophages).
  • Evaluation of CNV lesion size in genetically modified mice and pharmacologically treated mice (e.g., β3 receptor antagonist, splenic denervation/splenectomy).
  • Adoptive transfer of specific macrophage subtypes.

Main Results:

  • Ly6Chi macrophages/monocytes, but not lymphocytes, significantly exacerbated CNV.
  • CNV lesion size was reduced by β3 receptor antagonist treatment, splenic denervation, and splenectomy.
  • Splenic denervation and splenectomy decreased intraocular Ly6Chi macrophages.
  • Adoptive transfer of spleen-derived Ly6Chi cells increased CNV lesion size in splenic-denervated mice.

Conclusions:

  • Ly6Chi macrophages/monocytes play a crucial role in promoting CNV.
  • Sympathetic activity contributes to CNV, likely by enhancing the recruitment of macrophages to the eye.
  • Targeting sympathetic pathways or macrophage recruitment may be a therapeutic approach for CNV.