Vitamin D receptor (VDR) expression has been detected in many mammalian
tissues. Abundant evidence suggests a role of vitamin D in ocular function and
dysfunction, including immunological responses, glaucoma, myopia, and age-related
macular degeneration. It is still unclear, however, whether a VDR is expressed in the
mammalian retina in vivo,In this study, I sought to identify sites of VDR expression in
the adult mouse retina and to compare the structure of the retina and its major cell
types between wild type and VDRΔ/Δ mutant mice to determine the effects of the lack
of a functional VDR.
X-gal (β-galactosidase) histochemistry and lacZ immunohistochemistry were used to
detect lacZ reporter gene expression in the retina of adult VDRΔ/ΔlacZ mice
supplemented with calcium, phosphorus, and lactose. DAPI staining and immunohistochemistry
with retinal cell type-specific markers were performed on frozen
sections of wild type and VDRΔ/ΔlacZ mouse retinae.
In the adult mouse retina, VDR is expressed in the proximal inner nuclear layer and
in the ganglion cell layer. The VDRΔ/Δ mutation does not affect retinal layering and the
structure of the major retinal cell types. In the retina of VDRΔ/Δ mutant mice, parvalbumin
expression in a subset of amacrine and ganglion cells is significantly lower
compared to wild type controls. This is similar to findings in the kidney of VDR null
mice. In one week old mice, the VDRΔ/Δ mutation appears to be associated with
increased apoptosis. Together, the data suggest a role of vitamin D signaling in
amacrine and ganglion cell function.