Abstract
Purpose::
One of the pathological complications of Age-related macular degeneration (AMD) is Choroidal angiogenesis or Choroidal Neovascularization (CNV). The aim of this study was to investigate the role of adiponectin (APN) in mouse model of laser induced CNV.
Methods::
CNV was induced by laser photocoagulation in C57BL/6 mouse with Argon laser. Retinal pigment epithelium (RPE)-choroid-scleral flat mounts prepared from harvested eyes on day 1, 3, 5, and 7 post-laser were stained for elastin and the incidence of CNV was determined by confocal microscopy. mRNA levels of ßactin, VEGF, -FGF and APN were detected by RT-PCR. Quantification of APN in RPE-choroid tissue was accomplished by Western blot analysis. Mice were treated i.p. with 25 µg of recombinant APN or 50 µg of peptide 24 h prior to laser photocoagulation and every day until day 6 post-laser. Another set of animals received a single intravitreal injection of 2 µg of recombinant APN or 30 µg of APN peptide on the day of laser. Control group was given sterile PBS. The expression of Adiponectin, adiponectin receptors 1 (AdipoR1) and 2 (AdipoR2) was studied by immunohistochemistry.
Results::
We have shown by immunohistochemistry that the APN, AdipoR1 and AdipoR2 were expressed in normal mouse choroid. APN and AdipoR1 gradually increased during development of CNV. The expression of VEGF and ßFGF was inhibited in the laser spots (at day 3 post-laser) in APN treated mice. Compared to control mice the size of CNV complex was inhibited by 70% by intravitreal injection of APN and APN peptide and by 80% in the animals treated i.p. with these molecules.
Conclusions::
Our results demonstrate that APN plays an important role in choroidal angiogenesis and may have therapeutic implications in the treatment of CNV or wet type AMD.
Keywords: age-related macular degeneration • choroid: neovascularization • pathology: experimental