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High salt loading alters the expression and localization of glial aquaporins in rat retina.
Exp Eye Res. 2009 Jun 15; 89(1):88-94.EE

Abstract

In the neural retina, glial cells control the ionic concentrations in part by mediation of transmembrane water fluxes through aquaporin (AQP) water channels. The expression and immunolocalization of two water channels, AQP1 and AQP4, in the rat retina during experimental high salt loading were investigated in this study. Six-week-old Wistar rats were allowed free access to rat chow with 8% NaCl concentration. Of these rats, 6 were killed after 2, 6, 10 and 20 weeks. Twelve-week-old and 26-week-old Wistar rats with a normal diet (0.5% NaCl concentration) were used as controls. Retinal tissues were collected. Ultrathin sections stained with uranyl acetate and lead citrate were photographed using a transmission electron microscope (TEM). Retinal whole mounts and cryosections were immunostained with AQP1 and AQP4 antibodies to detect the immunolocalization changes by confocal microscopy. The AQP1 and AQP4 contents 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 the retinas of high salt loading animals, obvious intracellular edema was observed by TEM in retinal ganglion cell (RGC) and mitochondria swelling was observed in glial cells. Strong expression of AQP1 was found in glial cells located in the innermost retinal layers, mainly in astrocytes. The superficial retinal vessels were surrounded by AQP4 in control retinas, but by both AQP4 and AQP1 in retina of high salt loading animals. A similar alteration in the localization of AQP1 has been described in the rat retina after transient ischemia and diabetes. Western blot results supported the conclusion that the AQP1 expression increased during high salt diet. Our findings indicate that high salt loading may induce neural retina edema, and that altered glial cell-mediated water transport via AQP channels in the retina may be one of the reasons for intracellular edema in the neural retina.

Authors+Show Affiliations

EENT Hospital, Eye Institute, Fudan University, Fenyang Road 83, Shanghai, China.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

19268466

Citation

Qin, Yaowu, et al. "High Salt Loading Alters the Expression and Localization of Glial Aquaporins in Rat Retina." Experimental Eye Research, vol. 89, no. 1, 2009, pp. 88-94.
Qin Y, Fan J, Ye X, et al. High salt loading alters the expression and localization of glial aquaporins in rat retina. Exp Eye Res. 2009;89(1):88-94.
Qin, Y., Fan, J., Ye, X., Xu, G., Liu, W., & Da, C. (2009). High salt loading alters the expression and localization of glial aquaporins in rat retina. Experimental Eye Research, 89(1), 88-94. https://doi.org/10.1016/j.exer.2009.02.017
Qin Y, et al. High Salt Loading Alters the Expression and Localization of Glial Aquaporins in Rat Retina. Exp Eye Res. 2009 Jun 15;89(1):88-94. PubMed PMID: 19268466.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - High salt loading alters the expression and localization of glial aquaporins in rat retina. AU - Qin,Yaowu, AU - Fan,Jiawen, AU - Ye,Xiaofeng, AU - Xu,Gezhi, AU - Liu,Wei, AU - Da,Cuidi, Y1 - 2009/03/04/ PY - 2008/12/03/received PY - 2009/02/20/revised PY - 2009/02/24/accepted PY - 2009/3/10/entrez PY - 2009/3/10/pubmed PY - 2009/10/9/medline SP - 88 EP - 94 JF - Experimental eye research JO - Exp Eye Res VL - 89 IS - 1 N2 - In the neural retina, glial cells control the ionic concentrations in part by mediation of transmembrane water fluxes through aquaporin (AQP) water channels. The expression and immunolocalization of two water channels, AQP1 and AQP4, in the rat retina during experimental high salt loading were investigated in this study. Six-week-old Wistar rats were allowed free access to rat chow with 8% NaCl concentration. Of these rats, 6 were killed after 2, 6, 10 and 20 weeks. Twelve-week-old and 26-week-old Wistar rats with a normal diet (0.5% NaCl concentration) were used as controls. Retinal tissues were collected. Ultrathin sections stained with uranyl acetate and lead citrate were photographed using a transmission electron microscope (TEM). Retinal whole mounts and cryosections were immunostained with AQP1 and AQP4 antibodies to detect the immunolocalization changes by confocal microscopy. The AQP1 and AQP4 contents 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 the retinas of high salt loading animals, obvious intracellular edema was observed by TEM in retinal ganglion cell (RGC) and mitochondria swelling was observed in glial cells. Strong expression of AQP1 was found in glial cells located in the innermost retinal layers, mainly in astrocytes. The superficial retinal vessels were surrounded by AQP4 in control retinas, but by both AQP4 and AQP1 in retina of high salt loading animals. A similar alteration in the localization of AQP1 has been described in the rat retina after transient ischemia and diabetes. Western blot results supported the conclusion that the AQP1 expression increased during high salt diet. Our findings indicate that high salt loading may induce neural retina edema, and that altered glial cell-mediated water transport via AQP channels in the retina may be one of the reasons for intracellular edema in the neural retina. SN - 1096-0007 UR - https://www.unboundmedicine.com/medline/citation/19268466/High_salt_loading_alters_the_expression_and_localization_of_glial_aquaporins_in_rat_retina_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0014-4835(09)00055-4 DB - PRIME DP - Unbound Medicine ER -