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Sentaro Kusuhara, Sho Nobuyoshi, Keiko Kojima, Wataru Matsumiya, Makoto Nakamura; Mrp4 deficiency has no apparent effect on age-related changes of the mouse retina. Invest. Ophthalmol. Vis. Sci. 2016;57(12):2709.
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© 2017 Association for Research in Vision and Ophthalmology.
Mrp4 (multidrug resistance protein 4) is an energy-dependent membrane transporter responsible for cellular efflux of a broad range of xenobiotics and physiological substrates. As Mrp4 functions in maintaining physiological homeostasis by adjusting the intracellular level of bioactive substances, its deficiency might lead to tissue/organ damage under certain stress. Accordingly, the aim of this study is to investigate the Mrp4 roles in age-related alterations of the mouse retina using Mrp4 knockout mice.
Mrp4-/- mice and wild type (WT) mice were reared in the same condition to 8-12 weeks old (adult) or 10-12 months old (retire). The eye balls were harvested and one eye was prepared for retinal whole-mount fluorescein immunohistochemistry (IHC) and the other for retinal IHC for frozen section. Immunostaining was performed for CD31 (endothelial cell marker), GFAP (astrocyte marker), glutamine synthetase (Muller cell marker), and calbindin D-28K (marker for amacrine cell and horizontal cell). Retinal phenotypes were compared between Mrp4-/- mice and WT mice in each age group (n=4).
In adult mice, whole-mount IHC showed no apparent change between Mrp4-/- mice and WT mice in immunoreactivity for CD31 and GFAP and in the morphology of immunostained cells. Likewise, IHC for frozen section did not reveal any obvious phenotypic change in the cells stained for glutamine synthetase or calbindin D-28K in Mrp4-/- mice as compared to WT mice. In retire mice, the same results were obtained: retinal phenotypes in Mrp4-/- mice were similar to those in WT mice.
It is presumed that Mrp4 deficiency does not exert any noticeable influence on age-related retinal changes.
This is an abstract that was submitted for the 2016 ARVO Annual Meeting, held in Seattle, Wash., May 1-5, 2016.
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