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G. Ortiz, R. Bernard, E. Gabison, A. Rendon, J.-A. Sahel, R. Tadayoni; Dystrophin 71 a Membrane Cytoskeleton Protein Involved in Corneal Neovascularization. Invest. Ophthalmol. Vis. Sci. 2010;51(13):64.
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© ARVO (1962-2015); The Authors (2016-present)
The objective of this study is to investigate whether Dp71 the smallest product of Duchenne muscular dystrophy (DMD) gene, and key component of the membrane associated cytoskeleton plays a modulator role in corneal neovascularization (CNV).
The study of CNV was performed on Wild-Type C57BL6 (WT) and Dp71-null mice. CNV was induced by alkali injury in both strains and the mice were sacrified 7 days after. Neovascularization was observed in corneal flatmounts using vessel immunostaining with the CD31 antibody. The degree of angiogenesis was analyzed using Photoshop Cs. The influence of Dp71 on the expression of VEGF was quantified using an Elisa Kit. Expression of Dp71 in the cornea was analyzed by Western blot with a panspecific antibody against dystrophins (H4).
An increase of mean percentage corneal surface covered by CNV was observed in Dp71-null mice compared to WT mice, respectively 40.72% vs. 26.33%. (P<0.005). In WT mice, no increase of Dp71 during cornea neovascularization compared to a healthy cornea was found. It was observed also in WT that Dystrophin Dp116, normally expressed in the peripheral nervous system was present in the cornea. Moreover in the absence of Dp71 the Dp116 was up-regulated when compared with the WT mice strain. The concentrations of VEGF, a pro-angiogenic factor were higher in vascularized corneas of Dp71-null compared to WT mice.
The results suggest that dystrophin Dp71 could play a role in the modulation of corneal neovascularization
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