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Martin Glosmann, Theresa Kreilmeier, Ute Zeitz, Reinhold G. Erben; Vitamin D Receptor Expression in the Adult Mouse Retina. Invest. Ophthalmol. Vis. Sci. 2011;52(14):924.
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Ample evidence suggests a role of vitamin D in ocular function and dysfunction, including immune privilege, glaucoma, and age-related macular degeneration. However, little is known regarding vitamin D signaling in the adult retina. We sought to map vitamin D receptor (VDR) expression in the mouse retina and to determine the effects of a lack of a functional VDR on the structure of the retina and its major cell types.
X-Gal histochemistry and β-galactosidase immunohistochemistry were used to detect lacZ reporter gene expression in the retina of adult VDR mutant mice in which a lacZ reporter gene is driven by the endogenous VDR promoter (Mol. Endocrinol. 16: 1524-1534, 2002). The mice were kept on a rescue diet enriched with calcium, phosphorus, and lactose. DAPI staining and immunohistochemistry with retinal cell type-specific markers was performed on frozen sections of wildtype and VDR mutant mouse retinas.
In the adult VDR mutant mouse retina, lacZ reporter gene expression was confined to the proximal inner nuclear layer and to the ganglion cell layer. Adult VDR mutant and wildtype mice did not differ in retinal layering and the organization of the major retinal cell types. Parvalbumin immunosignal in a subset of amacrine and ganglion cells was significantly weaker in VDR mutant mice compared to wildtype controls.
In the adult mouse retina, VDR is expressed in the ganglion cell layer and the proximal inner nuclear layer. This suggests a role of vitamin D signaling in amacrine and ganglion cell function.
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