title: High-salt loading exacerbates increased retinal content of aquaporins AQP1 and AQP4 in rats with diabetic retinopathy.
abstract: In the neural retina, glial cells control formation of ionic gradients by mediating transmembrane water fluxes through aquaporin (AQP) water channels. Retinal content and immunolocalization of two water channels, AQP1 and AQP4, in the diabetic rat retinas during high-salt loading were examined in this study. Diabetes was induced by an intraperitoneal injection of streptozotocin. Diabetic and control animals were observed after varying lengths of exposure to normal- and high-salt conditions. Ultrathin sections of retinal tissue, stained with uranyl acetate and lead citrate, were photographed using a transmission electron microscope (TEM). Retinal wholemounts were immunostained with AQP1 and AQP4 antibody to detect the immunolocalization changes by confocal microscopy. AQP1 and AQP4 content were evaluated by Western blot analysis. In the retinas of high-salt loading diabetic animals, obviously increased intracellular edema was observed by TEM in ganglion cells and mitochondrial swelling was observed in glial cells. Immunolocalization of AQP1 increased from the posterior to peripheral retina. Western blot results indicated that a high-salt diet may cause increased retinal content of AQP4 and may exacerbate increased retinal content of AQP1 caused by diabetic retinopathy. High-salt loading may increase neural retinal edema in rats with diabetic retinopathy, and altered glial cell mediated water transport via AQP channels in the retina may play an important role in the neural retinal edema formation and resolution.
authors: EENT Hospital, Eye Institute, Fudan University, Fengyang Road 83, Shanghai 200031, China.
authors: Yaowu
authors: Y
authors: Qin
authors: Gezhi
authors: G
authors: Xu
authors: Jiawen
authors: J
authors: Fan
authors: Rachel E
authors: RE
authors: Witt
authors: Cuidi
authors: C
authors: Da
mesh_terms: D000818:Animals; D051398:Aquaporin 1 / Q000378:metabolism*; D051401:Aquaporin 4 / Q000378:metabolism*; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure; D015153:Blotting, Western; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000150:complications* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D003930:Diabetic Retinopathy / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D007150:Immunohistochemistry; D008297:Male; D018613:Microscopy, Confocal; D046529:Microscopy, Electron, Transmission; D008933:Mitochondrial Swelling / Q000187:drug effects; D009457:Neuroglia / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D010211:Papilledema / Q000209:etiology* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar; D012160:Retina / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D017673:Sodium Chloride, Dietary / Q000633:toxicity*; D013997:Time Factors; D015854:Up-Regulation; D014867:Water / Q000378:metabolism; D014882:Water-Electrolyte Balance
chemical_list: C496022:Aqp1 protein, rat; C496032:Aqp4 protein, rat; D051401:Aquaporin 4; D001786:Blood Glucose; D005904:Glial Fibrillary Acidic Protein; D017673:Sodium Chloride, Dietary; D014867:Water; D051398:Aquaporin 1