Purchase this article with an account.
L. J. Thomas, C. Meschter, C. S. Cook, G. Fava, R. A. Hammond, C. W. Rittershaus, H. C. Marsh, Jr.; Inhibition of Laser-Induced Choroidal Neovascularization in Rats by Soluble Complement Receptor Type 1 (TP10, sCR1). Invest. Ophthalmol. Vis. Sci. 2007;48(13):1765.
Download citation file:
© ARVO (1962-2015); The Authors (2016-present)
sCR1 is an inhibitor of the complement cascade. To investigate the potential of sCR1 in age-related macular degeneration we utilized a laser-induced retinopathy model in Brown Norway rats.
Following treatment (see below), retinae were lased with a 130 mW, 75 um spot size, 0.1 sec duration, applied to 9-, 12- and 3-oâ€TMclock positions, 2-3 disk diameters from the optic nerve of each eye. Rupture of the Bruch's membrane was identified by bubble formation. The fundus was photographed at the time of lasing and at necropsy. Animals were sacrificed two weeks post-lasing. For fluorescein angiography, FITC-dextran was administered by intracardiac injection immediately prior to euthanizing. Following sacrifice, one eye from each animal was fixed and processed for histological examination; the other eye was fixed in Davidsonâ€TMs Solution formalin so the retina could be prepared as a fixed whole mount.
As indicated below, neovascular lesions were induced by the laser procedure in all control animals. In animals receiving systemic sCR1, however, 5 of 12 rats developed no evidence of neovascular lesions.
Histopathologic examination by light microscopy of the retina indicated that both triamcinolone acetonide administration, and sCR1 administration for 5 days resulted in a reduction in the thickness of the neovascular plaque suggesting a positive therapeutic effect with both agents.
This PDF is available to Subscribers Only