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J.P. Jeanny, G. Soubrane, F. Behar-Cohen, R.A. Bejjani, L. Jonet, S. Thomasseau, D. Benezra; The Role of NOS II in Retinal Wound Healing After Choroidal Ischemia . Invest. Ophthalmol. Vis. Sci. 2003;44(13):3062.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: Study the influence of the NOS II gene on the retinal wound healing processes of the mouse eye after localized ischemia of the choroid. Methods: Wild type C57Bl6/Sev129 mice (WT) and NOS II knock out (KO) mice, underwent a standard photocoagulation protocol aimed at focally occluding the choroid blood supply. After pupil dilatation, krypton laser (50um spot size, 0.05'', 400mW) fundal lesions were created. Twelve WT and 12 KO mice received one single choroidal lesion located one to two disc diameters nasal to the optic nerve in both eyes. Two mice from each group were sacrificed 1, 3, 7, 14, 21 and 30 days after photocoagulation. One eye of each mouse was mounted in OCT and processed for immunohistochemical analysis using Lectin and specific antibodies for GFAP or von-Willebrand factor. TUNEL reaction was also carried out along with DAPI staining. The second eye was fixed in 4% PAF and processed for histology. A systematic analysis of the cellular remodelling processes within the laser lesion and its vicinity were carried out during the various time intervals. Results: After the first and 3rd day following the laser burn, few intact cells are observed within the choroid lesion. GFAP positive staining is observed within the wound. This staining is associated with cells originating from the retina. At the lesion edges, choroidal vessels and choriocappillaries are engorged. Histology of the tissues overlying the affected choroid demonstrated a gradual posterior invagination of the retinal inner and outer nuclear layers towards the choroid. These early alterations took a definite shape and pattern during the tested later time points. No major differences between the two groups of mice was observed. The GFAP positive cells (Muller's and glia) activation which followed the photocoagulation was also similar in both groups. The remodelling behaviour of the retinal and choroidal vessels was also analysed. In both tissues these processes behaved in a similar pattern in the WT and KO mice. On histology observations and after specific immuno stainings, only a few inflammatory cells from the reticulo-endothelial system were detected at the wound site. Conclusions: Deficiency of the NOS II gene expression does not appear to influence the general retinal and choroidal remodeling processes following laser photocoagulation. As no angiogenic processes were observed in this model under our conditions, it is not possible to speculate on the role of NOS II gene in this process.
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