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C. Dot, V. Parier, F. Behar–Cohen, D. Ben–Ezra, F. Sennlaub, L. Jonet, F. May, J.–C. Jeanny; Retinochoroidal Healing Processes After Argon Photocoagulation in Mice of Different Genetic Status . Invest. Ophthalmol. Vis. Sci. 2006;47(13):1426.
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© ARVO (1962-2015); The Authors (2016-present)
Analyse the influence of genetic status on the wound healing processes taking place following argon laser photocoagulation (PC) in mice eyes. Provide an approach for aetiology of age related macular degeneration, in an experimental model of choroidal neovascularization (CNV) which is validated especially in C57BL/6J mice.
Young adult C57BL/6J, wild type C57Bl6/Sev129, DBA, CBA, C3H/Hen (rd1), and rd10 mice underwent a standard argon laser PC protocol (one burn,50µm, 400mW, 0.05sec). Three animals were sacrificed by carbon hydroxide inhalation at different times after PC. The eyes were mounted in Tissue tek (OCT), snap frozen and processed for immuno–histochemistry with specific antibodies against GFAP, von Willebrand (vW) factor, F4/80 and KI67 . TUNEL reaction was also carried out along with DAPI to localise cells undergoing apoptosis. Flat mounts of the neuroretina and of the remaining retinal pigment epithelium–choroid–sclera complex were also prepared, incubated with TRITC–conjugated lectin Bandeiraea simplicifolia and anti–GFAP or vW antibodies and examined with a confocal microscope.
In all different types of mice, argon photocoagulation creates disruption of the RPE and Bruch’s membrane. In C57BL/6J mice we observe an intense staining with GFAP associated with activated retina astrocytes and Müller cells mostly in the center of the laser beam. Apoptotic cells are observed mostly located in the retinal outer nuclear layer, this reaction reaches its peak on day 3 . On day 7, new capillaries of choroidal origin initially detected at the external edges of the laser lesion, arise from the disrupted RPE and Bruch’s membrane and infiltrate the retina. These processes are accompanied during the first 7 days after photocoagulation by the infiltration of F4/80+ cells and KI67+ cells within the lesion . Under this conditions of photocoagulation, no evidence of CNV is observed in C57BL6/Sev 129 mice and in the retinal degeneration models except for CBA. On the contrary an intense choroidal vascular reaction is detected in DBA model, most important than in the previous validated C57BL/6J model.
Bruch’s membrane rupture previously required for CNV development appears to be a necessary but non sufficient condition. The genetic status influence a lot CNV development. This can support the inflammatory hypothesis of CNV. The role of photoreceptors must be evaluated too.
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