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Y. Qin, J. Fan, G. Xu; High Salt Loading Alters the Expression and Localization of Glial Aquaporins in Rat Retina. Invest. Ophthalmol. Vis. Sci. 2009;50(13):2908.
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© ARVO (1962-2015); The Authors (2016-present)
In the neural retina, the ion and osmohomeostasis is controlled by glial cells, in part by mediation of transmembrane water fluxes through aquaporin (AQP) water channels.In this study we investigated whether the expression and immunolocalization of two water channels, AQP1 and AQP4, alters in the rat retina during experimental high salt loading.
Six week old wistar rats were maintained to free access to rat chow with 8% Nacl and killed after 2, 6,10 and 20 weeks. Twelve and 26 week old normal wistar rats were set as control. Retinal tissues were collected. Ultrathin sections stained with uranyl acetate and lead citrate were photographed using an transmission electron microscope (TEM). Retinal wholemounts and cryosetion were immunostained with AQP1 and AQP4 antibody to detect the immunolocation changes under confocal microscope and the AQP1 and AQP4 content were evaluated by western blot analysis .
In control tissues, no intracellular edema and mitochondria swelling were observed by TEM. The immunoreactive AQP4 was expressed by glial cells (Müller cells and astrocytes) predominantly in the inner retina, and AQP1 was expressed in the outer retina. In retina of high salt loading animals, obvious intracellular edema was observed by TEM in retinal ganglion cell and mitochondria swelling were observed in Müller cells. Additional strong expression of AQP1 was found in glial cells located in the innermost retinal layers, mainly in astrocytes. A similar alteration in the localization of AQP1 has been described in the rat retina after transient ischemia and diabetes. Western blot results showed that the AQP1 expression level had linear linkage with the duration of high salt diet .
The data suggests that high salt loading induce the neural retina edema and the aquaporins -mediated water transport in the retina is altered especially at the superficial vessel plexus, that may be one of the reasons of intracellular edema in neural retina.
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