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Attenuation of choroidal neovascularization by β(2)-adrenoreceptor antagonism

Jeremy A Lavine1, Yanzhi Sang, Shoujian Wang

  • 1Departments of Ophthalmology and Visual Science, University of Wisconsin School of Medicine and Public Health, Madison, WI 53792, USA.

JAMA Ophthalmology
|January 11, 2013
PubMed
Abstract

Insights

Beta-adrenergic blockade significantly reduced choroidal neovascularization (CNV) in mice. This inhibition is mediated by β2-adrenoreceptors, which regulate vascular endothelial growth factor (VEGF) expression, offering a potential new treatment for CNV.

Area of Science:

  • Ophthalmology
  • Pharmacology
  • Molecular Biology

Background:

  • Choroidal neovascularization (CNV) is a leading cause of vision loss.
  • Current treatments for CNV have limitations.
  • The role of β-adrenergic signaling in CNV is not fully understood.

Purpose of the Study:

  • To investigate the effect of β-adrenergic blockade on laser-induced CNV in a mouse model.
  • To elucidate the mechanism by which β-adrenoreceptor antagonism inhibits CNV.

Main Methods:

  • Laser-induced CNV model in C57BL/6j mice.
  • Treatment with propranolol hydrochloride, a β-adrenergic blocker.
  • Assessment of neovascularization using ICAM-2 immunofluorescence.
  • Investigation of VEGF expression in choroidal endothelial cells (ChECs) and retinal pigment epithelial (RPE) cells.

Main Results:

  • Propranolol treatment resulted in a 50% reduction in laser-induced CNV.
  • Norepinephrine stimulated VEGF mRNA and protein in ChECs and RPE cells.
  • This stimulation was mediated by β2-adrenoreceptors.

Conclusions:

  • β-adrenergic blockade effectively inhibits CNV.
  • β2-adrenoreceptors play a key role in regulating VEGF expression in the choroid and RPE.
  • β-adrenergic antagonists may offer a novel therapeutic strategy for CNV.

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